Previously considered a topic for further research exploration, binge eating disorder was included in the "Diagnostic and Statistical Manual of Mental Disorders" in 2013. Until 2013, binge eating disorder was categorized as an Eating Disorder Not Otherwise Specified, an umbrella category for eating disorders that don't fall under the categories for anorexia nervosa or bulimia nervosa. Because it was not a recognized psychiatric disorder in the "DSM-IV" until 2013, it has been difficult to obtain insurance reimbursement for treatments. The disorder now has its own category under "DSM-5", which outlines the signs and symptoms that must be present to classify a person's behavior as binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.

According to DSM-5, the following criteria must be present to make a diagnosis of binge eating disorder. Studies have confirmed the high predictive value of these criteria for diagnosing BED.

A. Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:

1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of food that is definitely larger than what most people would eat in a similar period of time under similar circumstances.

2. A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).

B. The binge-eating episodes are associated with three (or more) of the following:

1. Eating much more rapidly than normal.

2. Eating until feeling uncomfortably full.

3. Eating large amounts of food when not feeling physically hungry.

4. Eating alone because of feeling embarrassed by how much one is eating.

5. Feeling disgusted with oneself, depressed, or very guilty afterward.

C. Marked distress regarding binge eating is present.

D. The binge eating occurs, on average, at least once a week for 3 months.

E. The binge eating is not associated with the recurrent use of inappropriate compensatory behavior as in bulimia nervosa and does not occur exclusively during the course of bulimia nervosa or anorexia nervosa.

The 2017 update to the American version of the ICD-10 includes BED under F50.81. ICD-11 may contain a dedicated entry (6B62), defining BED as frequent, recurrent episodes of binge eating (once a week or more over a period of several months) which are not regularly followed by inappropriate compensatory behaviors aimed at preventing weight gain.

Few studies to date have examined OSFED prevalence. The largest community study is by Stice (2013), who examined 496 adolescent females who completed annual diagnostic interviews over 8 years. Lifetime prevalence by age 20 for OSFED overall was 11.5%. 2.8% had atypical AN, 4.4% had subthreshold BN, 3.6% had subthreshold BED, and 3.4% had purging disorder. Peak age of onset for OSFED was 18–20 years. NES was not assessed in this study, but estimates from other studies suggest that it presents in 1% of the general population.

A few studies have compared the prevalence of EDNOS and OSFED and found that though the prevalence of atypical eating disorders decreased with the new classification system, the prevalence still remains high. For example, in a population of 215 young patients presenting for ED treatment, the diagnosis of EDNOS to OSFED decreased from 62.3% to 32.6%. In another study of 240 females in the U.S. with a lifetime history of an eating disorder, the prevalence changed from 67.9% EDNOS to 53.3% OSFED. Although the prevalence appears to reduce when using the categorizations of EDNOS vs. OSFED, a high proportion of cases still receive diagnoses of atypical eating disorders, which creates difficulties in communication, treatment planning, and basic research.

Few studies guide the treatment of individuals with OSFED. However, cognitive behavioral therapy (CBT), which focuses on the interplay between thoughts, feelings, and behaviors, has been shown to be the leading evidence-based treatment for the eating disorders of BN and BED. For OSFED, a particular cognitive behavioral treatment can be used called CBT-Enhanced (CBT-E), which was designed to treat all forms of eating disorders. This method focuses not only what is thought to be the central cognitive disturbance in eating disorders (i.e., over-evaluation of eating, shape, and weight), but also on modifying the mechanisms that sustain eating disorder psychopathology, such as perfectionism, core low self-esteem, mood intolerance, and interpersonal difficulties. CBT-E showed effectiveness in two studies (total N = 219) and well maintained over 60-week follow-up periods. CBT-E is not specific to individual types of eating disorders but is based on the concept that common mechanisms are involved in the persistence of atypical eating disorders, AN, and BN.

There are a number of management options for bedwetting. The following options apply when the bedwetting is not caused by a specifically identifiable medical condition such as a bladder abnormality or diabetes. Treatment is recommended when there is a specific medical condition such as bladder abnormalities, infection, or diabetes. It is also considered when bedwetting may harm the child's self-esteem or relationships with family/friends. Only a small percentage of bedwetting is caused by a specific medical condition, so most treatment is prompted by concern for the child's "emotional" welfare. Behavioral treatment of bedwetting overall tends to show increased self-esteem for children.

Parents become concerned much earlier than doctors. A study in 1980 asked parents and physicians the age that children should stay dry at night. The average parent response was 2.75 years old, while the average physician response was 5.13 years old.

Punishment is not effective and can interfere with treatment.

DSPD is genetically linked to attention deficit hyperactivity disorder by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD.

Thorough history regarding frequency of bedwetting, any period of dryness in between, associated daytime symptoms, constipation, and encopresis should be sought.

In medicine, insomnia is widely measured using the Athens insomnia scale. It is measured using eight different parameters related to sleep, finally represented as an overall scale which assesses an individual's sleep pattern.

A qualified sleep specialist should be consulted for the diagnosis of any sleep disorder so the appropriate measures can be taken. Past medical history and a physical examination need to be done to eliminate other conditions that could be the cause of insomnia. After all other conditions are ruled out a comprehensive sleep history should be taken. The sleep history should include sleep habits, medications (prescription and non-prescription), alcohol consumption, nicotine and caffeine intake, co-morbid illnesses, and sleep environment. A sleep diary can be used to keep track of the individual's sleep patterns. The diary should include time to bed, total sleep time, time to sleep onset, number of awakenings, use of medications, time of awakening and subjective feelings in the morning. The sleep diary can be replaced or validated by the use of out-patient actigraphy for a week or more, using a non-invasive device that measures movement.

Workers who complain of insomnia should not routinely have polysomnography to screen for sleep disorders. This test may be indicated for patients with symptoms in addition to insomnia, including sleep apnea, obesity, a thick neck diameter, or high-risk fullness of the flesh in the oropharynx. Usually, the test is not needed to make a diagnosis, and insomnia especially for working people can often be treated by changing a job schedule to make time for sufficient sleep and by improving sleep hygiene.

Some patients may need to do an overnight sleep study to determine if insomnia is present. Such a study will commonly involve assessment tools including a polysomnogram and the multiple sleep latency test. Specialists in sleep medicine are qualified to diagnose disorders within the, according to the ICSD, 81 major sleep disorder diagnostic categories. Patients with some disorders, including delayed sleep phase disorder, are often mis-diagnosed with primary insomnia; when a person has trouble getting to sleep and awakening at desired times, but has a normal sleep pattern once asleep, a circadian rhythm disorder is a likely cause.

In many cases, insomnia is co-morbid with another disease, side-effects from medications, or a psychological problem. Approximately half of all diagnosed insomnia is related to psychiatric disorders. In depression in many cases "insomnia should be regarded as a co-morbid condition, rather than as a secondary one;" insomnia typically predates psychiatric symptoms. "In fact, it is possible that insomnia represents a significant risk for the development of a subsequent psychiatric disorder." Insomnia occur in between 60% and 80% of people with depression. This may partly be due to treatment used for depression.

Determination of causation is not necessary for a diagnosis.

Obstructive sleep apnea (OSA) affects around 4% of men and 2% of women in the United States. In general, this disorder is more prevalent among men. However, this difference tends to diminish with age. Women experience the highest risk for OSA during pregnancy. Also, they tend to report experiencing depression and insomnia in conjunction with obstructive sleep apnea. In a meta-analysis of the various Asian countries, India and China present the highest prevalence of the disorder. Specifically, about 13.7% of the Indian population and 7% of Hong-Kong's population is estimated to have OSA. The two groups experience daytime OSA symptoms such as difficulties concentrating, mood swings, or high blood pressure, at similar rates (prevalence of 3.5% and 3.57%, respectively).

DSPD is diagnosed by a clinical interview, actigraphic monitoring, and/or a sleep diary kept by the patient for at least two weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea. If a person can adjust to a normal daytime schedule on her/his own, with just the help of alarm clocks and will-power, the diagnosis is not given.

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPD is often confused with: psychophysiological insomnia; depression; psychiatric disorders such as schizophrenia, ADHD or ADD; other sleep disorders; or school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders.

Due to rapidly increasing knowledge about sleep in the 20th century, including the discovery of REM sleep in the 1950s and circadian rhythm disorders in the 70s and 80s, the medical importance of sleep was recognized. The medical community began paying more attention than previously to primary sleep disorders, such as sleep apnea, as well as the role and quality of sleep in other conditions. By the 1970s in the USA, clinics and laboratories devoted to the study of sleep and sleep disorders had been founded, and a need for standards arose.

Specialists in Sleep Medicine were originally certified by the American Board of Sleep Medicine, which still recognizes specialists. Those passing the Sleep Medicine Specialty Exam received the designation "diplomate of the ABSM." Sleep Medicine is now a recognized subspecialty within internal medicine, family medicine, pediatrics, otolaryngology, psychiatry and neurology in the United States. Certification in Sleep Medicine shows that the specialist:"has demonstrated expertise in the diagnosis and management of clinical conditions that occur during sleep, that disturb sleep, or that are affected by disturbances in the wake-sleep cycle. This specialist is skilled in the analysis and interpretation of comprehensive polysomnography, and well-versed in emerging research and management of a sleep laboratory."

Competence in sleep medicine requires an understanding of a myriad of very diverse disorders, many of which present with similar symptoms such as excessive daytime sleepiness, which, in the absence of volitional sleep deprivation, "is almost inevitably caused by an identifiable and treatable sleep disorder", such as sleep apnea, narcolepsy, idiopathic hypersomnia, Kleine–Levin syndrome, menstrual-related hypersomnia, idiopathic recurrent stupor, or circadian rhythm disturbances. Another common complaint is insomnia, a set of symptoms which can have a great many different causes, physical and mental. Management in the varying situations differs greatly and cannot be undertaken without a correct diagnosis.

Sleep dentistry (bruxism, snoring and sleep apnea), while not recognized as one of the nine dental specialties, qualifies for board-certification by the American Board of Dental Sleep Medicine (ABDSM). The resulting Diplomate status is recognized by the American Academy of Sleep Medicine (AASM), and these dentists are organized in the Academy of Dental Sleep Medicine (USA). The qualified dentists collaborate with sleep physicians at accredited sleep centers and can provide oral appliance therapy and upper airway surgery to treat or manage sleep-related breathing disorders.

In the UK, knowledge of sleep medicine and possibilities for diagnosis and treatment seem to lag. Guardian.co.uk quotes the director of the Imperial College Healthcare Sleep Centre: "One problem is that there has been relatively little training in sleep medicine in this country – certainly there is no structured training for sleep physicians." The Imperial College Healthcare site shows attention to obstructive sleep apnea syndrome (OSA) and very few other sleep disorders. Some NHS trusts have specialist clinics for respiratory and/or neurological sleep medicine.

Going to sleep and waking up at the same time every day can create a steady pattern which may help to prevent or treat insomnia. Avoidance of vigorous exercise and any caffeinated drinks a few hours before going to sleep is recommended, while exercise earlier in the day is beneficial. The bedroom should be cool and dark, and the bed should only be used for sleep and sex. These are some of the points included in what doctors call "sleep hygiene".

Clinical definition of enuresis is urinary incontinence beyond age of 4 years for daytime and beyond 6 years for nighttime, or loss of continence after three months of dryness.

Current DSM-IV-TR criteria:

- Repeated voiding of urine into bed or clothes (whether involuntary or intentional)

- Behavior must be clinically significant as manifested by either a frequency of twice a week for at least three consecutive months or the presence of clinically significant distress or impairment in social, academic (occupational), or other important areas of functioning.

- Chronological age is at least 5 years of age (or equivalent developmental level).

- The behavior is not due exclusively to the direct physiological effect of a substance (such as a diuretic) or a general medical condition (such as diabetes, spina bifida, a seizure disorder, etc.).

All these criteria must be met in order to diagnose an individual.

Many children overcome incontinence naturally (without treatment) as they grow older. The number of cases of incontinence goes down by 15 percent for each year after the age of 5.

Because a number of parasomnias may be confused with RBD, it is necessary to conduct formal sleep studies such as polysomnography (PSG) performed at sleep centers that are experienced in evaluating parasomnias in order to establish a diagnosis. In RBD, a single night of extensive monitoring of sleep, brain, and muscle activity will almost always reveal the lack of muscle paralysis during REM sleep, and it will also eliminate other causes of parasomnias.

Recently, due to the limited access to PSG, attempts have been made to identify RBD from clinical interview as well as questionnaires. Postuma et al. have validated a single-question screening tool for RBD (RBD1Q) that could be easily applied in general practice to the patient and their bed partner. A positive answer to the RBDQ1, ‘Have you ever been told or suspected yourself, that you seem to act out your dreams while asleep (for example, punching, flailing your arms in the air, making running movement etc.)?’ should encourage the medical practitioner to consider the diagnosis of RBD as it offers good sensitivity (94%) and specificity (87%). Other questionnaires, such as the Rapid Eye Movement (REM) sleep Behavior Disorder Screening Questionnaire (RBDSQ) or the REM Sleep Behavior Questionnaires – Hong-Kong are available for more detailed characterisation.

Possible treatments for circadian rhythm sleep disorders include:

- Behavior therapy or advice about sleep hygiene where the patient is told to avoid naps, caffeine, and other stimulants. They are also told to not be in bed for anything besides sleep and sex.

- Dark therapy, for example the use of blue-blocking goggles, is used to block blue- and bluegreen wavelength light from reaching the eye during evening hours so that the production of melatonin is not decreased or eliminated.

- Medications such as melatonin and modafinil (Provigil), or other short term sleep aids or wake-promoting agents can be beneficial; the former is a natural neurohormone responsible partly and in tiny amounts for the human body clock. The melatonin agonist Tasimelteon, trade name Hetlioz, has been approved in the USA solely for the treatment of non-24-hour sleep–wake disorder in totally blind people.

- Sleep phase chronotherapy may progressively advance or delay sleep time.

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.

Once diagnosed, ASPD can be treated with bright light therapy in the evenings or behaviorally with chronotherapy. Unlike other sleep disorders, ASPD does not disrupt normal functioning at work during the day and the patient does not complain of excessive daytime sleepiness. If their ASPD is causing people to lose out on evening activities, including putting their own typical children to bed, they may be able to force themselves to stay up later than their circadian rhythm requires. A sufferer of ASPD will still wake up very early and if this cycle continues it can lead to chronic sleep deprivation and other sleep disorders.

Major changes in the management of daytime wetting came about in the 1990s. In most current programs, non-invasive treatments incorporate hydration, timed voiding, correction of constipation and in some cases, computer assisted pelvic floor retraining. These methods have been extremely successful in correcting daytime wetting. Bladder stretching exercises (where the person tries to hold their urine as long as possible) are no longer recommended. In fact, some urologists actually believe that this can be dangerous because the person could develop the long-term habit of tightening the urethral sphincter muscle, which can cause bladder or kidney problems. Urinating on a regular basis is much preferred.

Ruling out infections can also be a part of the differential.

The most comprehensive assessment so far has estimated RBD prevalence to be about 0.5% in individuals aged 15 to 100. It is far more common in males: most studies report that only about a tenth of sufferers are female. This may partially be due to a referral bias, as violent activity carried out by men is more likely to result in harm and injury and is more likely to be reported than injury to male bed partners by women, or it may reflect a true difference in prevalence as a result of genetic or androgenic factors. The mean age of onset is estimated to be about 60 years.

Various conditions are very similar to RBD in that sufferers exhibit excessive sleep movement and potentially violent behavior. Such disorders include sleepwalking and sleep terrors, which are associated with other stages of sleep, nocturnal seizures and obstructive sleep apnea which can induce arousals from REM sleep associated with complex behaviors. Because of the similarities between the conditions, polysomnography plays an important role in confirming RBD diagnosis.

It is now apparent that RBD appears in association with a variety of different conditions. Narcolepsy has been reported as a related disorder. Both RBD and narcolepsy involve dissociation of sleep states probably arising from a disruption of sleep control mechanisms. RBD has also been reported following cerebrovascular accident and neurinoma (tumor), indicating that damage to the brain stem area may precipitate RBD. RBD is usually chronic. However, it may be acute and sudden in onset if associated with drug treatment or withdrawal (particularly with alcohol withdrawal). 60% of RBD is idiopathic. This includes RBD that is found in association with conditions such as Parkinson's disease and dementia with Lewy bodies, where it is often seen to precede the onset of neurodegenerative disease. Monoamine oxidase inhibitors, tricyclic antidepressants, Selective serotonin reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD.

One of these disorders is extrinsic (from Latin "extrinsecus", from without, on the outside) or circumstantial:

- Shift work sleep disorder, which affects people who work nights or rotating shifts.

Formerly, jet lag, too, was classified as an extrinsic type circadian rhythm disorder.

Families who are impacted by SIDS should be offered emotional support and grief counseling. The experience and manifestation of grief at the loss of an infant are impacted by cultural and individual differences.

In 1999, Louis Ptáček's and Ying-Hui Fu's research group at the University of California, San Francisco reported findings of a human circadian rhythm disorder showing a familial tendency. The disorder was characterized by a lifelong pattern of sleep onset around 7:30 p.m. and offset around 4:30 a.m. Among three lineages, 29 people were identified as affected with this familial advanced sleep-phase disorder (FASPD), and 46 were considered unaffected. The pedigrees demonstrated FASPD to be a highly penetrant, autosomal dominant trait.

Two years after reporting the finding of FASPD, Ptáček's and Fu's groups published results of genetic sequencing analysis on a family with FASPD. They genetically mapped the FASPD locus to chromosome 2q where very little human genome sequence was then available. Thus, they identified and sequenced all the genes in the critical interval. One of these was Period2 (Per2). Sequencing of the hPer2 gene revealed a serine-to-glycine point mutation in the CKI binding domain of the hPER2 protein that resulted in hypophosphorylation of Per2 in vitro.

In 2005, Fu's and Ptáček's labs reported discovery of a different mutation causing FASPD. This time, CKIδ was implicated, demonstrating an A-to-G missense mutation that resulted in a threonine-to-alanine alteration in the protein. The evidence for both of these reported causes of FASPD is strengthened by the absence of said mutations in all tested control subjects and by demonstration of functional consequences of the respective mutations in vitro. Fruit flies and mice engineered to carry the human mutation also demonstrated abnormal circadian phenotypes although the mutant flies had a long circadian period while the mutant mice had a shorter period. The differences between flies and mammals that account for this difference are not known. Most recently, Ptáček and Fu reported additional studies of the human Per2 S662G mutation and generation of mice carrying the human mutation. These mice had a circadian period almost 2 hours shorter than wild-type animals. Genetic dosage studies of CKIδ on the Per2 S662G mutation revealed that CKIδ is having opposite effects on Per2 levels depending on the sites on Per2 that CKIδ is phosphorylating.

A large investigation into diphtheria-tetanus-pertussis vaccination and potential SIDS association by Berlin School of Public Health, Charité – Universitätsmedizin Berlin concluded: "Increased DTP immunisation coverage is associated with decreased SIDS mortality. Current recommendations on timely DTP immunisation should be emphasised to prevent not only specific infectious diseases but also potentially SIDS."

Many other studies have also reached conclusions that vaccinations reduce the risk of SIDS. Studies generally show that SIDS risk is approximately halved by vaccinations.

Parasomnias are a category of sleep disorders that involve abnormal movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or during arousal from sleep. Most parasomnias are dissociated sleep states which are partial arousals during the transitions between wakefulness and NREM sleep, or wakefulness and REM sleep.