Currently there are no clinically established laboratory investigations available to predict prognosis or therapeutic response.

Tumors in children who develop OMS tend to be more mature, showing favorable histology and absence of n-myc oncogene amplification than similar tumors in children without symptoms of OMS. Involvement of local lymph nodes is common, but these children rarely have distant metastases and their prognosis, in terms of direct morbidity and mortality effects from the tumor, is excellent. The three-year survival rate for children with non-metastatic neuroblastoma and OMS was 100% according to Children’s Cancer Group data (gathered from 675 patients diagnosed between 1980 and 1994); three-year survival in comparable patients with OMS was 77%. Although the symptoms of OMS are typically steroid-responsive and recovery from acute symptoms of OMS can be quite good, children often suffer lifelong neurologic sequelae that impair motor, cognitive, language, and behavioral development.

Most children will experience a relapsing form of OMS, though a minority will have a monophasic course and may be more likely to recover without residual deficits. Viral infection may play a role in the reactivation of disease in some patients who had previously experienced remission, possibly by expanding the memory B cell population. Studies have generally asserted that 70-80% of children with OMS will have long-term neurologic, cognitive, behavioral, developmental, and academic impairment. Since neurologic and developmental difficulties have not been reported as a consequence of neuroblastoma or its treatment, it is thought that these are exclusively due to the immune mechanism underlying OMS.

One study concludes that: ""Patients with OMA and neuroblastoma have excellent survival but a high risk of neurologic sequelae. Favourable disease stage correlates with a higher risk for development of neurologic sequelae. The role of anti-neuronal antibodies in late sequelae of OMA needs further clarification"."

Another study states that: ""Residual behavioral, language, and cognitive problems occurred in the majority"."

In children, most cases are associated with neuroblastoma and most of the others are suspected to be associated with a low-grade neuroblastoma that spontaneously regressed before detection. In adults, most cases are associated with breast carcinoma or small-cell lung carcinoma. It is one of the few paraneoplastic (meaning 'indirectly caused by cancer') syndromes that occurs in both children and adults, although the mechanism of immune dysfunction underlying the adult syndrome is probably quite different.

It is hypothesized that a viral infection (perhaps St. Louis encephalitis, Epstein-Barr, Coxsackie B, enterovirus, or just a flu) causes the remaining cases, though a direct connection has not been proven, or in some cases Lyme disease.

OMS is not generally considered an infectious disease. OMS is not passed on genetically.

Sexsomnia affects individuals of all age groups and backgrounds but present as an increased risk for individuals who possess the following:

- coexisting sleep disorders

- sleep disruption secondary to obstructive sleep apnea

- sleep related epilepsy

- certain medications

Behaviors of pelvic thrusting, sexual arousal, and orgasms are often attributed to sleep related epilepsy disorder. In some cases, physical contact with a partner in bed acted as a trigger to initiate sexsomia behaviors.

Medications, such as the commonly prescribed treatment for insomnia, Ambien, have been shown to induce symptoms commonly associated with sexsomnia.

Like sleep-related eating disorders, sexsomnia presents more commonly in adults than children. However, these individuals usually have a history of parasomnias that began during childhood.

Most girls can stay dry at night by age six and most boys stay dry by age seven. Boys are three times more likely to wet the bed than girls.

Doctors frequently consider bedwetting as a self-limiting problem, since most children will outgrow it. Children 5 to 9 years old have a spontaneous cure rate of 14% per year. Adolescents 10 to 18 years old have a spontaneous cure rate of 16% per year.

Approximate bedwetting rates are:

- Age 5: 20%

- Age 6: 10–15%

- Age 7: 7%

- Age 10: 5%

- Age 15: 1–2%

- Age 18–64: 0.5–1%

As can be seen from the numbers above, a portion of bedwetting children will not outgrow the problem. Adult rates of bedwetting show little change due to spontaneous cure. Persons who are still enuretic at age 18 are likely to deal with bedwetting throughout their lives.

Studies of bedwetting in adults have found varying rates. The most quoted study in this area was done in the Netherlands. It found a 0.5% rate for 18- to 64-year-olds. A Hong Kong study, however, found a much higher rate. The Hong Kong researchers found a bedwetting rate of 2.3% in 16- to 40-year-olds.

It is possible for an individual who suffers from sexsomnia to experience a variety of negative emotions due to the nature of their disorder. The following are commonly seen secondary effects of sexsomnia:

- Anger

- Confusion

- Denial

- Frustration

- Guilt

- Revulsion

- Shame

The effects of sexsomnia also extend to those in relationship with the sufferer. Whether the significant other is directly involved, in the case of sexual intercourse, or a bystander, in the case of masturbation behavior, they are often the first to recognize the abnormal behavior. These abnormal sexual behaviors may be unwanted by the partner, which could lead to the incident being defined as sexual assault.

In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.

Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.

The aetiology of NE is not fully understood, although there are three common causes: excessive urine volume, poor sleep arousal, and bladder contractions. Differentiation of cause is mainly based on patient history and fluid charts completed by the parent or carer to inform management options.

The following list summarizes bedwetting's known causes and risk factors. Enuretic patients frequently have more than one cause or risk factor from the items listed below.

Most cases of bedwetting are PNE-type, which has two related most common causes

- Neurological-developmental delay This is the most common cause of bedwetting. Most bedwetting children are simply delayed in developing the ability to stay dry and have no other developmental issues. Studies suggest that bedwetting may be due to a nervous system that is slow to process the feeling of a full bladder.

- Genetics Bedwetting has a strong genetic component. Children whose parents were not enuretic have only a 15% incidence of bedwetting. When one or both parents were bedwetters, the rates jump to 44% and 77% respectively. Genetic research shows that bedwetting is associated with the genes on chromosomes 13q and 12q (possibly 5 and 22 also).

These first two items are the most common factors in bedwetting, but current medical technology offers no easy testing for either cause. There is no test to prove that bedwetting is only a developmental delay, and genetic testing offers little or no benefit.

As a result, other conditions should be ruled out. The following causes are less common, but are easier to prove and more clearly treated:

- Alcohol consumption Drinking alcohol increases urine production, inhibits anti-diuretic hormone production, decreases awareness, increases drowsiness and causes impulsive decisions.

- Anti-diuretic hormone (ADH) Anti-diuretic hormone regulates urine production by increasing water reabsorption in the kidney. Both insufficient production of ADH, or insufficient response to ADH, leads to an overproduction of urine, often beyond the capacity of a child's bladder. The body normally increases ADH levels at night, signalling the kidneys to produce less urine. The diurnal change may not be seen until about age 10. In some bed wetting children this increase in ADH production does not occur, while other children may produce an increased amount of ADH but their response is insufficient.

- Attention deficit hyperactivity disorder (ADHD) Children with ADHD are 2.7 times more likely to have bedwetting issues.

- Caffeine Caffeine increases urine production.

- Constipation Chronic constipation can cause bed wetting. When the bowels are full, it can put pressure on the bladder. Often such children defecate normally, yet they retain a significant mass of material in the bowel which causes bed wetting.

- Infection/disease Infections and disease are more strongly connected with and with daytime wetting. Less than 5% of all bedwetting cases are caused by infection or disease, the most common of which is a urinary tract infection.

- More severe neurological-developmental issues Patients with intellectual disabilities have a higher rate of bedwetting problems. One study of seven-year-olds showed that "handicapped and intellectually disabled children" had a bedwetting rate almost three times higher than "non-handicapped children" (26.6% vs. 9.5%, respectively).

- Physical abnormalities Less than 10% of enuretics have urinary tract abnormalities, such as a smaller than normal bladder. Current data does support increased bladder tone in some enuretics, which functionally would decrease bladder capacity.

- Psychological Psychological issues (e.g., death in the family, sexual abuse, extreme bullying) are established as a cause of (a return to bedwetting), but are very rarely a cause of PNE-type bedwetting. Bedwetting can also be a symptom of a pediatric neuropsychological disorder called PANDAS. When enuresis is caused by a psychological or neuropsychological disorder, the bedwetting is considered a "symptom" of the disorder. Enuresis has a psychological diagnosis code (see previous section), but it is not considered a psychological condition itself. (See section on psychological/social impact, below)

- Sleep apnea Sleep apnea stemming from an upper airway obstruction has been associated with bedwetting. Snoring and enlarged tonsils or adenoids are a sign of potential sleep apnea problems.

- Sleepwalking Sleepwalking can lead to bedwetting. During sleepwalking, the sleepwalker may think he/she is in another room. When the sleepwalker urinates during a sleepwalking episode, he/she usually thinks they are in the bathroom, and therefore urinate where they think the toilet should be. Cases of this have included opening a closet and urinating in it; urinating on the sofa and simply urinating in the middle of the room.

- Stress Stress is not a cause of "primary" nocturnal enuresis (PNE), but is well established as a cause of returning to bedwetting (). Researchers studying children who have yet to stay dry find "no relationship to social background, life stresses, family constellation, or number of residencies." On the other hand, stress is a cause of people who return to wetting the bed. Researchers find that moving to a new town, parent conflict or divorce, arrival of a new baby, or loss of a loved one or pet can cause insecurity, contributing to returning bedwetting.

- Type 1 Diabetes Mellitus Nocturnal enuresis could be the presenting symptom of type 1 diabetes mellitus, classically associated with polyuria, polydipsia, and polyphagia; weight loss, lethargy, and diaper candidiasis may also be present in those with new-onset disease.

Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.

Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.

Daytime wetting is more common in girls than in boys, but bedwetting is three times as prevalent in boys (i.e., around 75% of sufferers are male). At the age of 7 approximately 3% of girls and 2% of boys experience functional daytime wetting at least once a week.

The effects of myoclonus in an individual can vary depending on the form and the overall health of the individual. In severe cases, particularly those indicating an underlying disorder in the brain or nerves, movement can be extremely distorted and limit ability to normally function, such as in eating, talking, and walking. In these cases, treatment that is usually effective, such as clonazepam and sodium valproate, may instead cause adverse reaction to the drug, including increased tolerance and a greater need for increase in dosage. However, the prognosis for more simple forms of myoclonus in otherwise healthy individuals may be neutral, as the disease may cause few to no difficulties. Other times the disease starts simply, in one region of the body, and then spreads.

According to the American Academy of Sleep Medicine there is a wide range of potential causes, including anxiety, caffeine, stress and strenuous activities in the evening. However, most hypnic jerks occur essentially at random in healthy people.

Another hypothesis is evolutionary, stretching back to our primate ancestors. A study at the University of Colorado has suggested that a hypnic jerk could be "an archaic reflex to the brain's misinterpretation of muscle relaxation with the onset of sleep as a signal that a sleeping primate is falling out of a tree. The reflex may also have had selective value by having the sleeper readjust or review his or her sleeping position in a nest or on a branch in order to assure that a fall did not occur."

During an epilepsy and intensive care study, the lack of a preceding spike discharge measured on an epilepsy monitoring unit, along with the presence only at sleep onset, helped differentiate hypnic jerks from epileptic myoclonus.

According to a study on sleep disturbances in the "Journal of Neural Transmission", a hypnic jerk occurs during the non-rapid eye movement sleep cycle and is an "abrupt muscle action flexing movement, generalized or partial and asymmetric, which may cause arousal, with an illusion of falling". Hypnic jerks are more frequent in childhood with 4 to 7 per hour in the age range from 8 to 12 years old, and they decrease toward 1 or 2 per hour by 65 to 80 years old.

Hyperekplexia ("exaggerated surprise") is a neurologic disorder classically characterised by pronounced startle responses to tactile or acoustic stimuli and hypertonia. The hypertonia may be predominantly truncal, attenuated during sleep and less prominent after a year of age. Classic hyperekplexia is caused by genetic mutations in a number of different genes, all of which play an important role in glycine neurotransmission. Glycine is used by the central nervous system as an inhibitory neurotransmitter. Hyperekplexia is generally classified as a genetic disease, but some disorders can mimic the exaggerated startle of hyperekplexia.

The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.

Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.

Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.

The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

The three main signs of hyperekplexia are generalized stiffness, excessive startle beginning at birth and nocturnal myoclonus. Affected individuals are fully conscious during episodes of stiffness, which consist of forced closure of the eyes and an extension of the extremities followed by a period of generalised stiffness and uncontrolled falling at times. Initially, the disease was classified into a "major" and a "minor" form, with the minor form being characterized by an excessive startle reflex, but lacking stiffness. There is only genetic evidence for the existence of the major form.

Other signs and symptoms of hyperekplexia may include episodic neonatal apnea, excessive movement during sleep and the head-retraction reflex. The link to some cases of Sudden Infant Death remains controversial.

PLMD is estimated to occur in approximately 4% of adults (aged 15–100), but is more common in the elderly, especially females, with up to 11% experiencing symptoms. PLMD appears to be related to restless legs syndrome (RLS) - a study of 133 people found that 80% of those with RLS also had PLMD. However the opposite is not true: many people who have PLMD do "not" also have restless legs syndrome.

The condition may be a sign of various disease states, including but not exclusive to the following:

- Cancers

- Lymphoma

- Leukemia

- Infections

- HIV/AIDS

- Tuberculosis

- Mycobacterium avium-intracellulare infection

- Infectious mononucleosis

- Fungal infections (histoplasmosis, coccidioidomycosis)

- Lung abscess

- Infective endocarditis

- Brucellosis

- Pneumocystis pneumonia (most often - in immunocompromised individuals)

- Endocrine disorders

- Menopause

- Premature ovarian failure

- Hyperthyroidism

- Diabetes mellitus (nocturnal hypoglycemia)

- Endocrine tumors (pheochromocytoma, carcinoid)

- Orchiectomy

- Rheumatic disorders

- Takayasu's arteritis

- Temporal arteritis

- Other

- Obstructive sleep apnea

- Gastroesophageal reflux disease

- Chronic fatigue syndrome

- Fibromyalgia

- Granulomatous disease

- Chronic eosinophilic pneumonia

- Lymphoid hyperplasia

- Diabetes insipidus

- Prinzmetal's angina

- Anxiety

- Pregnancy

- Drugs

- Antipyretics (salicylates, acetaminophen)

- Antihypertensives

- Dinitrophenol - a common side effect

- Phenothiazines

- Drug withdrawal: ethanol, benzodiazepines, heroin (and other opiates),

- Over-bundling

- Autonomic over-activity

- IBD (inflammatory bowel disease) - Crohn's disease/ulcerative colitis

Prognosis is poor, however, current analysis suggests that those associated with thymoma, benign or malignant, show a less favorable prognosis (CASPR2 Ab positive).

It is mostly unknown what causes PLMD, but in many cases the patient also suffers from other medical problems such as Parkinson's disease or narcolepsy. Factors that increase the likelihood of PLMD in the absence of restless leg syndrome include being a shift worker, snoring, coffee drinking, stress, and use of hypnotics, particularly in the case of benzodiazepine withdrawal. For women, the presence of musculoskeletal disease, heart disease, obstructive sleep apnea, cataplexy, doing physical activities close to bedtime and the presence of a mental disorder were significantly associated with having a higher risk of both PLMD and restless legs syndrome.

Over the past thirty years, several studies have found that those afflicted with NSRED all have different symptoms and behaviors specific to them, yet they also all have similar characteristics that doctors and psychologists have identified to distinguish NSRED from other combinations of sleep and eating disorders such as night eating syndrome. Winkelman says that typical behaviors for patients with NSRED include: "Partial arousals from sleep, usually within 2 to 3 hours of sleep onset, and subsequent ingestion of food in a rapid or 'out of control' manner." They also will attempt to eat bizarre amalgamations of foods and even potentially harmful substances such as glue, wood, or other toxic materials. In addition, Schenck and Mahowald noted that their patients mainly ate sweets, pastas, both hot and cold meals, improper substances such as "raw, frozen, or spoiled foods; salt or sugar sandwiches; buttered cigarettes; and odd mixtures prepared in a blender."

During the handling of this food, patients with NSRED distinguish themselves, as they are usually messy or harmful to themselves. Some eat their food with their bare hands while others attempt to eat it with utensils. This occasionally results in injuries to the person as well as other injuries. After completing their studies, Schenck and Mahowald said, "Injuries resulted from the careless cutting of food or opening of cans; consumption of scalding fluids (coffee) or solids (hot oatmeal); and frenzied running into walls, kitchen counters, and furniture." A few of the more notable symptoms of this disorder include large amounts of weight gain over short periods of time, particularly in women; irritability during the day, due to lack of restful sleep; and vivid dreams at night. It is easily distinguished from regular sleepwalking by the typical behavioral sequence consisting of "rapid, 'automatic' arising from bed, and immediate entry into the kitchen." In addition, throughout all of the studies done, doctors and psychiatrists discovered that these symptoms are invariant across weekdays, weekends, and vacations as well as the eating excursions being erratically spread throughout a sleep cycle. Most people that suffer from this disease retain no control over when they arise and consume food in their sleep. Although some have been able to restrain themselves from indulging in their unconscious appetites, some have not and must turn to alternative methods of stopping this disorder. It is important for trained physicians to recognize these symptoms in their patients as quickly as possible, so those with NSRED may be treated before they injure themselves.

Research on myoclonus is supported through the National Institute of Neurological Disorders and Stroke (NINDS). The primary focus of research is on the role of neurotransmitters and receptors involved in the disease. Identifying whether or not abnormalities in these pathways cause myoclonus may help in efforts to develop drug treatments and diagnostic tests. Determining the extent that genetics play in these abnormalities may lead to potential treatments for their reversal, potentially correcting the loss of inhibition while enhancing mechanisms in the body that would compensate for their effects.

For those patients who have not been able to stop this disorder on their own, doctors have been working to discover a treatment that will work for everyone. One treatment that Schenck and Mahowald studied consisted of psychotherapy combined with "environmental manipulation". This was usually done separately from the weight-reducing diets. However, during this study only 10 percent of the patients were able to lose more than one third of their initial excess weight, which was not a viable percentage. In addition, they reported that many of the patients experienced "major depression" and "severe anxiety" during the attempted treatments. This was not one of the most successful attempts to help those with NSRED.

However, Dr. R. Auger reported on another trial treatment where patients were treated utilizing pramipexole. Those conducting the treatment noticed how the nocturnal median motor activity was decreased, as was assessed by actigraphy, and individual progress of sleep quality was reported. Nevertheless, Augur also said, "27 percent of subjects had RLS (restless legs syndrome, a condition known to respond to this medication), and number and duration of waking episodes related to eating behaviors were unchanged." Encouraged by the positive response verified in the above-mentioned trial treatment, doctors and psychiatrists conducted a more recent study described by Auger as "efficacy of topiramate [an antiepileptic drug associated with weight loss] in 17 consecutive patients with NSRED." Out of the 65 percent of patients who continued to take the medication on a regular basis, all confirmed either considerable development or absolute remission of "night-eating" in addition to "significant weight loss" being achieved. This has been one of the most effective treatments discovered so far, but many patients still suffered from NSRED. Therefore, other treatments were sought after.

Such treatments include those targeted to associated sleep disorders with the hope that it would play an essential part of the treatment process of NSRED. In Schenck and Mahowald's series, combinations of cardibopa/L-dopa, codeine, and clonazepam were used to treat five patients with RLS and one patient with somnambulism and PLMS (periodic limb movements in sleep). These patients all were suffering from NSRED as well as these other disorders, and they all experienced a remission of their NSRED as a result of taking these drugs. Two patients with OSA (obstructive sleep apnea) and NSRED also reported as having a "resolution of their symptoms with nasal continuous positive airway pressure (nCPAP) therapy." Clonazepam monotherapy was also found to be successful in 50 percent of patients with simultaneous somnambulism. Interestingly, dopaminergic agents such as monotherapy were effective in 25 percent of the NSRED subgroup. Success with combinations of dopaminergic and opioid drugs, with the occasional addition of sedatives, also was found in seven patients without associated sleep disorders. In those for whom opioids and sedatives are relatively contraindicated (e.g., in those with histories of substance abuse), two case reports were described as meeting with success with a combination of bupropion, levodopa, and trazodone. Notably, hypnotherapy, psychotherapy, and various behavioral techniques, including environmental manipulation, were not effective on the majority of the patients studied. Nevertheless, Auger argue that behavioral strategies should complement the overall treatment plan and should include deliberate placement of food to avoid indiscriminate wandering, maintenance of a safe sleep environment, and education regarding proper sleep hygiene and stress management. Even with their extensive studies, Schenck and Mahowald did not find the success as Auger found by treating his patients with topiramate.

Most common cause of autoimmune encephalitis after acute demyelinating encephalitis in England. More than 500 cases have been reported in literature till 2013. In California Encephalitis Project it was found >4 times as frequently as herpes simplex virus type 1 (HSV-1), varicella-zoster virus (VZV), and West Nile virus (WNV). Among patients with first-onset schizophrenia incidence varies between 6–10%.

- Age – frequently 5–76 years, Median age of patients was 23 years

- Sex – 80% Female

Two international research studies are currently underway. The International Genetic Study done with the Spinner Laboratory at The Children's Hospital of Philadelphia studies the ring 20 chromosome at the molecular level. The Clinical Research Study collects clinical information from parents to create a database of about the full spectrum of patients with ring chromosome 20 syndrome.

RHS type 1 is caused by the impairment of a regulatory mechanism between cerebellar and brainstem nuclei and has been associated with a wide range of diseases, including Lafora disease, dentatorubropallidoluysian atrophy, and celiac disease.