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.

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.

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.

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.

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.

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

Favorable response to treatment with the ADHD drug methylphenidate (Ritalin) has been reported, but this treatment option is not acceptable to all patient families.

Dr. Lane Robson, of The Children’s Clinic in Calgary, Alberta, says "If a child is having a wetting episode once a month, medicating them daily is probably not a good treatment. If it’s a daily issue, you may have to make that decision."

Episodes of giggle incontinence are embarrassing and socially incapacitating, diminishing the quality of life. Those having the condition learn to adapt by avoiding activities that may bring on laughter. Other approaches include limiting fluid intake, trying to remain seated, and concealing leakage by wearing absorbent pads and dark clothing.

Patients with incontinence should be referred to a medical practitioner specializing in this field. Urologists specialize in the urinary tract, and some urologists further specialize in the female urinary tract. A urogynecologist is a gynecologist who has special training in urological problems in women. Family physicians and internists see patients for all kinds of complaints, and are well trained to diagnose and treat this common problem. These primary care specialists can refer patients to urology specialists if needed.

A careful history taking is essential especially in the pattern of voiding and urine leakage as it suggests the type of incontinence faced. Other important points include straining and discomfort, use of drugs, recent surgery, and illness.

The physical examination will focus on looking for signs of medical conditions causing incontinence, such as tumors that block the urinary tract, stool impaction, and poor reflexes or sensations, which may be evidence of a nerve-related cause.

A test often performed is the measurement of bladder capacity and residual urine for evidence of poorly functioning bladder muscles.

Other tests include:

- Stress test – the patient relaxes, then coughs vigorously as the doctor watches for loss of urine.

- Urinalysis – urine is tested for evidence of infection, urinary stones, or other contributing causes.

- Blood tests – blood is taken, sent to a laboratory, and examined for substances related to causes of incontinence.

- Ultrasound – sound waves are used to visualize the kidneys, ureters, bladder, and urethra.

- Cystoscopy – a thin tube with a tiny camera is inserted in the urethra and used to see the inside of the urethra and bladder.

- Urodynamics – various techniques measure pressure in the bladder and the flow of urine.

Patients are often asked to keep a diary for a day or more, up to a week, to record the pattern of voiding, noting times and the amounts of urine produced.

Research projects that assess the efficacy of anti-incontinence therapies often quantify the extent of urinary incontinence. The methods include the 1-h pad test, measuring leakage volume; using a voiding diary, counting the number of incontinence episodes (leakage episodes) per day; and assessing of the strength of pelvic floor muscles, measuring the maximum vaginal squeeze pressure.

Globally, up to 35% of the population over the age of 60 years is estimated to be incontinent.

In 2014, urinary leakage affected between 30% and 40% of people over 65 years of age living in their own homes or apartments in the U.S. Twenty-four percent of older adults in the U.S. have moderate or severe urinary incontinence that should be treated medically.

Bladder control problems have been found to be associated with higher incidence of many other health problems such as obesity and diabetes. Difficulty with bladder control results in higher rates of depression and limited activity levels.

Incontinence is expensive both to individuals in the form of bladder control products and to the health care system and nursing home industry. Injury related to incontinence is a leading cause of admission to assisted living and nursing care facilities. More than 50% of nursing facility admissions are related to incontinence.

According to one meta-analysis, the mean prevalence rate for North America and Western Europe is estimated to be 14.5±8.0%. Specifically in the United States, the prevalence of restless leg syndrome is estimated to be between 5 and 15.7% when using strict diagnostic criteria. RLS is over 35% more prevalent in American women than their male counterparts.

If the patient presents with acute hyponatraemia (overhydration) caused by psychogenic polydipsia, treatment usually involves administration of intravenous hypertonic (3%) saline until the serum sodium levels stabilise to within a normal range, even if the patient becomes asymptomatic.

Treatment for psychogenic polydipsia depends on severity and may involve behavioural and pharmacological modalities.

A systematic review states 7.6% of the general population experiences sleep paralysis at least once in their lifetime. Its prevalence among men is 15.9% while 18.9% of women experience it. When considering specific populations, 28.3% of students and 31.9% of psychiatric patients have experienced this phenomenon at least once in their lifetime. Of those psychiatric patients, 34.6% have panic disorder. Sleep paralysis in students is slightly more prevalent for those of Asian descent (39.9%) than other ethnicities (Hispanic: 34.5%, African descent: 31.4%, Caucasian 30.8%).

The ICSD-R listed diagnostic criteria for sleep bruxism. The minimal criteria include both of the following:

- A. symptom of tooth-grinding or tooth-clenching during sleep, and

- B. One or more of the following:

- Abnormal tooth wear

- Grinding sounds

- Discomfort of the jaw muscles

With the following criteria supporting the diagnosis:

- C. polysomnography shows both:

- Activity of jaw muscles during sleep

- No associated epileptic activity

- D. No other medical or mental disorders (e.g., sleep-related epilepsy, which may cause abnormal movement during sleep).

- E. The presence of other sleep disorders (e.g., obstructive sleep apnea syndrome).

Early diagnosis of bruxism is advantageous, due to the possible damage that may be incurred and the detrimental effect on quality of life. A diagnosis of bruxism is usually made clinically, and is mainly based on the person's history (e.g. reports of grinding noises) and the presence of typical signs and symptoms, including tooth mobility, tooth wear, masseteric hypertrophy, indentations on the tongue, hypersensitive teeth (which may be misdiagnosed as reversible pulpitis), pain in the muscles of mastication, and clicking or locking of the temporomandibular joints. Questionnaires can be used to screen for bruxism in both the clinical and research settings.

For tooth grinders who live in same household with other people, diagnosis of grinding is straightforward: Housemates or family members would advise a bruxer of recurrent grinding. Grinders who live alone can likewise resort to a sound-activated tape recorder. To confirm the condition of clenching, on the other hand, bruxers may rely on such devices as the Bruxchecker, Bruxcore, or a beeswax-bearing biteplate.

The Individual (personal) Tooth-Wear Index was developed to objectively quantify the degree of tooth wear in an individual, without being affected by the number of missing teeth. Bruxism is not the only cause of tooth wear. Another possible cause of tooth wear is acid erosion, which may occur in people who drink a lot of acidic liquids such as concentrated fruit juice, or in people who frequently vomit or regurgitate stomach acid, which itself can occur for various reasons. People also demonstrate a normal level of tooth wear, associated with normal function. The presence of tooth wear only indicates that it had occurred at some point in the past, and does not necessarily indicate that the loss of tooth substance is ongoing. People who clench and perform minimal grinding will also not show much tooth wear. Occlusal splints are usually employed as a treatment for bruxism, but they can also be of diagnostic use, e.g. to observe the presence or absence of wear on the splint after a certain period of wearing it at night.

The most usual trigger in sleep bruxism that leads a person to seek medical or dental advice is being informed by sleeping partner of unpleasant grinding noises during sleep. The diagnosis of sleep bruxism is usually straightforward, and involves the exclusion of dental diseases, temporomandibular disorders, and the rhythmic jaw movements that occur with seizure disorders (e.g. epilepsy). This usually involves a dental examination, and possibly electroencephalography if a seizure disorder is suspected. Polysomnography shows increased masseter and temporalis muscular activity during sleep. Polysomnography may involve electroencephalography, electromyography, electrocardiography, air flow monitoring and audio–video recording. It may be useful to help exclude other sleep disorders; however, due to the expense of the use of a sleep lab, polysomnography is mostly of relevance to research rather than routine clinical diagnosis of bruxism.

Tooth wear may be brought to the person's attention during routine dental examination. With awake bruxism, most people will often initially deny clenching and grinding because they are unaware of the habit. Often, the person may re-attend soon after the first visit and report that they have now become aware of such a habit.

Several devices have been developed that aim to objectively measure bruxism activity, either in terms of muscular activity or bite forces. They have been criticized for introducing a possible change in the bruxing habit, whether increasing or decreasing it, and are therefore poorly representative to the native bruxing activity. These are mostly of relevance to research, and are rarely used in the routine clinical diagnosis of bruxism. Examples include the "Bruxcore Bruxism-Monitoring Device" (BBMD, "Bruxcore Plate"), the "intra-splint force detector" (ISFD), and electromyographic devices to measure masseter or temporalis muscle activity (e.g. the "BiteStrip", and the "Grindcare").

At the time of first PANS presentation, note any family history of pharyngitis, impetigo, perianal dermatitis, and GAS infections. If possible, family members should have a throat swab cultured for GAS. Ongoing vigilance against GAS infections in any of the patient’s close contacts is important, as symptom exacerbations have been reported following exposure to a sibling with GAS (even when the PANDAS patient had no evidence of infection). Prompt medical attention to symptoms suggestive of streptococcal infection is important not only to protect the patient, but also siblings, who may be at an increased genetic risk for PANS.

Additionally, studies have shown a high rate of concurrent autoimmunity in patients with PANS and their first degree family members further supporting a role for inflammation in PANS.

The majority of children with enuresis show no other symptoms besides wetting the bed at night. If other symptoms are present, such as blood stains in their underwear or unusual pain, the child is likely to have a more serious medical problem. Children with encopresis are likely to exhibit symptoms such as; loss of appetite, loose or watery stools, abdominal pain, scratching or itching of anal area because of irritation, withdrawal from friends, or secretive attitude associated with bowel movements.

Encopresis: The most common cause of Encopresis is constipation. When a child becomes constipated, feces build up in and stretch the rectum. This stretching causes the nerve endings to become dull. The child may not feel when he or she needs to eliminate the feces or if the waste is coming out. Inside the rectum, the feces could become too large or solid to eliminate without feeling pain. While the mass of feces is stuck in the child's rectum, liquid feces could leak from around the mass and out of the child's body. The main causes of constipation are diet, lack of sufficient amounts of water, stress, not enough exercise, and inconsistent bathroom routines.

Enuresis: The cause of Enuresis is thought to be unclear and usually is attributed to many factors.

- Genetic- there is a genetic component within Enuresis and it tends to run in families.

- Inability to feel that the bladder is full and be aroused from sleep.

- Insufficient size of bladder- the child's bladder is too small to contain the amount of urine produced.

- Psychological Factors- these are not main factors that contribute to Enuresis, but stress may be a cause.

- Maturational Delay- the child's recognition that the bladder is full and he or she needs to go to the bathroom is a developmental issue. Many children with Enuresis will develop this skill as they grow older.

Due to the condition's rarity, it is frequently misdiagnosed, often as cerebral palsy. This results in patients often living their entire childhood with the condition untreated.

The diagnosis of SS can be made from a typical history, a trial of dopamine medications, and genetic testing. Not all patients show mutations in the GCH1 gene (GTP cyclohydrolase I), which makes genetic testing imperfect.

Sometimes a lumbar puncture is performed to measure concentrations of biopterin and neopterin, which can help determine the exact form of dopamine-responsive movement disorder: early onset parkinsonism (reduced biopterin and normal neopterin), GTP cyclohydrolase I deficiency (both decreased) and tyrosine hydroxylase deficiency (both normal).

In approximately half of cases, a phenylalanine loading test can be used to show decreased conversion from the amino acid phenylalanine to tyrosine. This process uses BH4 as a cofactor.

During a sleep study (polysomnography), decreased twitching may be noticed during REM sleep.

An MRI scan of the brain can be used to look for conditions that can mimic SS (for example, metal deposition in the basal ganglia can indicate Wilson's disease or pantothenate kinase-associated neurodegeneration). Nuclear imaging of the brain using positron emission tomography (PET scan) shows a normal radiolabelled dopamine uptake in SS, contrary to the decreased uptake in Parkinson's disease.

Other differential diagnoses include metabolic disorders (such as GM2 gangliosidosis, phenylketonuria, hypothyroidism, Leigh disease) primarily dystonic juvenile parkinsonism, autosomal recessive early onset parkinsonism with diurnal fluctuation, early onset idiopathic parkinsonism, focal dystonias, dystonia musculorum deformans and dyspeptic dystonia with hiatal hernia.

- Diagnosis - main

- typically referral by GP to specialist Neurological Hospital e.g. National Hospital in London.

- very hard to diagnose as condition is dynamic w.r.t. time-of-day AND dynamic w.r.t. age of patient.

- correct diagnosis only made by a consultant neurologist with a complete 24-hour day-cycle observation(with video/film) at a Hospital i.e. morning(day1)->noon->afternoon->evening->late-night->sleep->morning(day2).

- patient with suspected SS required to walk in around hospital in front of Neuro'-consultant at selected daytime intervals to observe worsening walking pattern coincident with increased muscle tension in limbs.

- throughout the day, reducing leg-gait, thus shoe heels catching one another.

- diurnal affect of condition: morning(fresh/energetic), lunch(stiff limbs), afternoon(very stiff limbs), evening(limbs worsening), bedtime(limbs near frozen).

- muscle tension in thighs/arms: morning(normal), lunch(abnormal), afternoon(very abnormal), evening(bad), bedtime(frozen solid).

- Diagnosis - additional

- lack of self-esteem at school/college/University -> eating disorders in youth thus weight gains.

- lack of energy during late-daytime (teens/adult) -> compensate by over-eating.

Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.

Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. and or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.

Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.

Sensory processing disorder since 1994 is accepted in the Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood (DC:0-3R) and is not recognized as a mental disorder in medical manuals such as the ICD-10 or the DSM-5.

Diagnosis is primarily arrived at by the use of standardized tests, standardized questionnaires, expert observational scales, and free play observation at an occupational therapy gym. Observation of functional activities might be carried at school and home as well. Some scales that are not exclusively used in SPD evaluations are used to measure visual perception, function, neurology and motor skills.

Depending on the country, diagnosis is made by different professionals, such as occupational therapists, psychologists, learning specialists, physiotherapists and/or speech and language therapists. In some countries it is recommended to have a full psychological and neurological evaluation if symptoms are too severe.

Treatment can include amoxicillin-clavulanic acid, intravenous fluid administration and paracetamol oral for pain relief. Other treatment varies based on the condition and extent of uropathy.

It is estimated that up to 16.5% of elementary school aged children present elevated SOR behaviors in the tactile or auditory modalities. However, this figure might represent an underestimation of Sensory Over Responsivity prevalence, since this study did not include children with developmental disorders or those delivered preterm, who are more likely to present it.

This figure is, nonetheless, larger than what previous studies with smaller samples had shown: an estimate of 5–13% of elementary school aged children.

Incidence for the remaining subtypes is currently unknown.