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.

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.

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.

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.

Symptoms of sexsomnia can be caused by or be associated with:

- stress factors

- sleep deprivation

- Consumption of alcohol or other drugs

- Pre-existing parasomnia behaviors

Sleep deprivation is known to have negative effects on the brain and behavior. Extended periods of sleep deprivation often results in the malfunctioning of neurons, directly effecting an individual's behavior. While muscles are able to regenerate even in the absence of sleep, neurons are incapable of this ability. Specific stages of sleep are responsible for the regeneration of neurons while others are responsible for the generation of new synaptic connections, the formation of new memories, etc.

Zolpidem, the widely known sedative Ambien, is used as common treatment for insomnia and has been seen to result in sexsomnia as an adverse effect.

Sexsomnia can also be triggered by physical contact initiated by a partner, or an individual sharing the same bed.

Histamine plays a role in wakefulness in the brain. An allergic reaction over produces histamine causing wakefulness and inhibiting sleep Sleep problems are common in people with allergic rhinitis. A study from the N.I.H. found that sleep is dramatically impaired by allergic symptoms and that the degree of impairment is related to the severity of those symptoms s Treatment of allergies has also been shown to help sleep apnea.

A hypnic jerk, hypnagogic jerk, sleep start, sleep twitch or night start is an involuntary twitch which occurs when a person is beginning to fall asleep, often causing them to awaken suddenly for a moment. Physically, hypnic jerks resemble the "jump" experienced by a person when startled, sometimes accompanied by a falling sensation. Hypnic jerks are associated with a rapid heartbeat, quickened breathing, sweat, and sometimes "a peculiar sensory feeling of 'shock' or 'falling into the void. A higher occurrence is reported in people with irregular sleep schedules.

A systematic review found that traumatic childhood experiences (such as family conflict or sexual trauma) significantly increases the risk for a number of sleep disorders in adulthood, including sleep apnea, narcolepsy, and insomnia. It is currently unclear whether or not moderate alcohol consumption increases the risk of obstructive sleep apnea.

In addition, an evidence-based synopses suggests that the sleep disorder, idiopathic REM sleep behavior disorder (iRBD), may have a hereditary component to it. A total of 632 participants, half with iRBD and half without, completed self-report questionnaires. The results of the study suggest that people with iRBD are more likely to report having a first-degree relative with the same sleep disorder than people of the same age and sex that do not have the disorder. More research needs to be conducted to gain further information about the hereditary nature of sleep disorders.

A population susceptible to the development of sleep disorders is people who have experienced a traumatic brain injury (TBI). Because many researchers have focused on this issue, a systematic review was conducted to synthesize their findings. According to their results, TBI individuals are most disproportionately at risk for developing narcolepsy, obstructive sleep apnea, excessive daytime sleepiness, and insomnia. The study's complete findings can be found in the table below:

Waking up in the middle of the night, or nocturnal awakening, is the most frequently reported insomnia symptom, with approximately 35% of Americans over 18 reporting waking up three or more times per week. Of those who experience nocturnal awakenings, 43% report difficulty in resuming sleep after waking, while over 90% report the condition persisting for more than six months. Greater than 50% contend with MOTN conditions for more than five years.

A 2008 "Sleep in America" poll conducted by the National Sleep Foundation found that 42% of respondents awakened during the night at least a few nights a week, and 29% said they woke up too early and couldn’t get back to sleep. Other clinical studies have reported between 25% and 35% of people experience nocturnal awakenings at least three nights a week.

Nocturnal awakenings are more common in older patients and have been associated with depressive disorders, chronic pain, obstructive sleep apnea, obesity, alcohol consumption, hypertension, gastroesophageal reflux disease, heart disease, menopause, prostate problems, and bipolar disorders.

Nocturnal awakenings can be mistaken as shift work disorder.

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.

Benign myoclonus can occur in healthy individuals and is most commonly caused by nothing other than arbitrary muscle contractions. Myoclonus may develop in response to infection, hyperosmolar hyperglycemic state, head or spinal cord injury, stroke, stress, brain tumors, kidney or liver failure, lipid storage disease, chemical or drug poisoning, as a side effect of certain drugs (such as tramadol, quinolones, benzodiazepine, gabapentin, sertraline, lamotrigine), or other disorders.

Benign myoclonic movements are commonly seen during the induction of general anesthesia with intravenous medications such as etomidate and propofol. These are postulated to result from decreased inhibitory signaling from cranial neurons. Prolonged oxygen deprivation to the brain, hypoxia, may result in posthypoxic myoclonus. People suffering from benign fasciculation syndrome can often experience myoclonic jerking of limbs, fingers and thumbs.

Myoclonus can occur by itself, but most often as one of several symptoms associated with a variety of nervous system disorders, including multiple sclerosis, Parkinson's disease, Alzheimer's disease, Opsoclonus Myoclonus, Creutzfeldt–Jakob disease, Lyme Disease and lupus. Myoclonic jerks commonly occur in persons with epilepsy, a disorder in which the electrical activity in the brain becomes disordered leading to seizures. It is also found in MERRF (Myoclonic Epilepsy with Ragged Red Fibers), a rare mitochondrial encephalomyopathy. Myoclonus can be a coexisting condition with Tourette syndrome.

Jerks of muscle groups, much of the body, or a series in rapid succession, which results in the person jerking bolt upright from a more relaxed sitting position is sometimes seen in ambulatory patients being treated with high doses of morphine, hydromorphine, and similar drugs, and is possibly a sign of high and/or rapidly increasing serum levels of these drugs. Myoclonic jerks caused by other opioids, such as tramadol and pethidine, may be less benign. Medications unrelated to opioids, such as anticholinergics, are known to cause myoclonic jerks.

Benign neonatal sleep myoclonus (BNSM) is the occurrence of myoclonus (jerky movements) during sleep. It is not associated with seizures.

Occurs in the first few weeks of life, usually resolves in first 2–3 months of life. Often worries parents because they appear like seizures, but they are not. Features that can help distinguish this condition from seizures include: The myoclonic movements only occur during sleep, when baby is woken up the myoclonic movements stop, normal EEG, normal neurological examination, normal developmental examination. The myoclonic jerks occur during non-REM sleep

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.

Myoclonic dystonia or Myoclonus dystonia syndrome is a rare movement disorder that induces spontaneous muscle contraction causing abnormal posture. The prevalence of myoclonus dystonia has not been reported, however, this disorder falls under the umbrella of movement disorders which affect thousands worldwide. Myoclonus dystonia results from mutations in the SGCE gene coding for an integral membrane protein found in both neurons and muscle fibers. Those suffering from this disease exhibit symptoms of rapid, jerky movements of the upper limbs (myoclonus), as well as distortion of the body's orientation due to simultaneous activation of agonist and antagonist muscles (dystonia).

Myoclonus dystonia is caused by loss-of-function-mutations in the epsilon sarcoglycan gene (SGCE). The disease is dominantly inherited, however SGCE is an imprinted gene, so only the paternal allele is expressed. Therefore, children suffering from this disease inherit the mutation from the father. If the mutated allele is inherited from the mother, the child is not likely to exhibit symptoms.

While no cure has been found for myoclonus dystonia, treatment options are available to those suffering from the disease. Ethanol often ameliorates the symptoms well, and so the syndrome is also called "Alcohol-responsive dystonia". Alcohol may be substituted by benzodiazepines, such as clonazepam, which work through the same mechanism. Deep brain stimulation (DBS) is another viable option that can alleviate symptoms without the unwanted side effects of medications, and has been successful in treating other movement disorders.

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.

Epidemiological studies of serotonin syndrome are difficult as many physicians are unaware of the diagnosis or they may miss the syndrome due to its variable manifestations. In 1998 a survey conducted in England found that 85% of the general practitioners that had prescribed the antidepressant nefazodone were unaware of serotonin syndrome. The incidence may be increasing as a larger number of pro-serotonergic drugs (drugs which increase serotonin levels) are now being used in clinical practice. One postmarketing surveillance study identified an incidence of 0.4 cases per 1000 patient-months for patients who were taking nefazodone. Additionally, around 14 to 16 percent of persons who overdose on SSRIs are thought to develop serotonin syndrome.

To date, there is no single, universal treatment that has been found to cure myoclonus dystonia. However, there are several treatment methods that have been found to be effective for helping to reduce the symptoms associated with the 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.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

Possible causes include:

- Syncope (fainting)

- Reflex anoxic seizures

- Breath-holding spells of childhood

- Hypoglycaemia

- Cataplexy

- Hyperekplexia, also called startle syndrome

- Migraine

- Narcolepsy

- Non-epileptic myoclonus

- Opsoclonus

- Parasomnias, including night terrors

- Paroxysmal kinesigenic dyskinesia

- Repetitive or ritualistic behaviours

- Tics

- AADC Deficiency

Non-epileptic seizures are paroxysmal events that mimic an epileptic seizure but do not involve abnormal, rhythmic discharges of cortical neurons. They are caused by either physiological or psychological conditions. The latter is discussed more fully in psychogenic non-epileptic seizures.

[Please could somebody add an actual description of what happens when somebody has a seizure or 'paroxysmal event'?!]

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.

Upon the discontinuation of serotonergic drugs, most cases of serotonin syndrome resolve within 24 hours, although in some cases delirium may persist for a number of days. Symptoms typically persist for a longer time frame in patients taking drugs which have a long elimination half-life, active metabolites, or a protracted duration of action.

Cases have reported muscle pain and weakness persisting for months, and antidepressant discontinuation may contribute to ongoing features. Following appropriate medical management, serotonin syndrome is generally associated with a favorable prognosis.

Common causes include, but not limited to:

- Incomplete emptying of the bladder

- Irritable bladder

- Constipation

- Stress

- Urinary tract infection

- Urgency (not “making it” to the bathroom in time)

- Anatomic abnormality

- Poor toileting habits

- Small bladder capacity

- Medical conditions like overactive bladder disorder