Abstract

Nocturnal enuresis is involuntary urination during sleep in a child old enough to have achieved reliable bladder control, conventionally five years; it is the clinical name for bedwetting. The modern account treats it not as a single disease but as the output of three partly independent systems: a night-time excess of urine, a bladder that holds too little, and a sleeping brain that fails to wake to a full bladder. Underlying the first is a blunted nocturnal rise in the antidiuretic hormone vasopressin, so that the kidneys produce more urine at night than the bladder can store. It is a cognitive-behavioural as well as a physiological condition, comorbid with attention-deficit/hyperactivity disorder and treated first by conditioning with an enuresis alarm. This article sets out its classification, the three-system model, its pathophysiology, epidemiology, and treatment, with interactive demonstrations.

Keywords: nocturnal enuresis, bedwetting, nocturnal polyuria, enuresis alarm

What Nocturnal Enuresis Is

Nocturnal enuresis is wetting that happens while a child is asleep, in a child who is past the age at which night-time dryness is normally established. The qualifier matters: continence is a developmental achievement, and a young child who is not yet dry at night is not enuretic in the clinical sense. By convention the line is drawn at five years of age, the point by which most children have reliable night-time control, so that wetting during sleep after that age is counted as a sign rather than a stage (Austin et al., 2016). It is the night-time member of a pair: enuresis in the broad sense covers involuntary urination that the child cannot yet control, and nocturnal enuresis is the sleeping form, set against the daytime form that occurs while the child is awake.

The modern vocabulary has sharpened this. The International Children's Continence Society, the body that standardises the terminology of childhood bladder problems, now reserves the word enuresis for wetting during sleep, precisely because the night-time and daytime signs have different mechanisms and different treatments (Austin et al., 2016; Nevéus et al., 2006). Whatever it is called, bedwetting is read the way a clinician reads any functional sign: not as a disease to be named and closed, but as evidence about how a child's urine production, bladder, and sleeping brain are working together through the night.

Key Takeaways
  • Nocturnal enuresis is involuntary wetting during sleep in a child past the age of expected bladder control, conventionally five years; it is the clinical term for bedwetting.
  • The modern three-system model explains it as a mismatch between night-time urine output, bladder capacity, and arousal from sleep.
  • Many children overproduce urine at night because the normal nocturnal rise in the antidiuretic hormone vasopressin is blunted, a state called nocturnal polyuria.
  • It is classified as monosymptomatic (sleep wetting alone) or non-monosymptomatic (with daytime bladder symptoms), and as primary or secondary.
  • First-line treatments are the enuresis alarm, a conditioning therapy with the most durable effect, and desmopressin, which replaces the missing night-time vasopressin.

The domain spans renal physiology, bladder function, and the sleep and arousal systems that link the two to waking behaviour. Table 1 sets out the principal ways nocturnal enuresis is classified, the basis of each distinction, and why it matters for treatment; the mechanistic sections that follow take them up in turn.

Table 1. Principal classifications of nocturnal enuresis, the basis of each, and its clinical significance.
Classification Basis of the distinction Clinical significance
MonosymptomaticSleep wetting with no daytime lower-urinary-tract symptoms.The straightforward form; responds well to alarm or desmopressin.
Non-monosymptomaticSleep wetting accompanied by daytime urgency, frequency, or incontinence.Daytime symptoms must be treated first; otherwise night-time treatment fails.
PrimaryThe child has never had a sustained dry period of six months.The common form, usually developmental in origin.
SecondaryWetting returns after at least six months of dryness.Prompts a look for a trigger: stress, infection, or new illness.

Classification: Types of Bedwetting

The clinical understanding of bedwetting rests on a shared vocabulary, and that vocabulary is the work of the International Children's Continence Society. Its standardisation documents fixed the definitions that every later study and guideline uses: what counts as enuresis, how to separate it from the daytime sign, and how to subclassify it (Nevéus et al., 2006). The 2010 document drew the single most consequential line, between monosymptomatic and non-monosymptomatic enuresis, and built the diagnostic pathway around it (Nevéus et al., 2010).

Two distinctions do most of the work. The first is between monosymptomatic nocturnal enuresis, sleep wetting in a child with no daytime bladder symptoms, and non-monosymptomatic nocturnal enuresis, where the night-time wetting is accompanied by daytime urgency, frequency, or incontinence. The distinction is not academic: in the non-monosymptomatic child the daytime problem must be assessed and treated first, because an overactive or dysfunctional bladder by day will defeat any night-time treatment (Nevéus et al., 2020; Vande Walle et al., 2012). The second distinction is between primary enuresis, in which the child has never achieved a sustained dry spell of six months, and secondary enuresis, in which bedwetting returns after a dry period. Primary enuresis is the common, developmental form; secondary enuresis prompts a search for a precipitant, such as psychological stress, a urinary tract infection, constipation, or newly emerged diabetes (Robson, 2009).

The Three-System Model

The organising idea of the modern field is that bedwetting is not one failure but the coincidence of up to three. The three-system model, set out as a conceptual framework by Butler and Holland, holds that a child wets at night when a problem in any of three partly independent systems tips the balance: the kidneys produce too much urine overnight, the bladder stores too little or contracts uninhibitedly, and the sleeping brain fails to rouse the child to the signal that the bladder is full or emptying (Butler & Holland, 2000). No single system is the cause; it is their interaction that matters. A child with mild nocturnal overproduction will stay dry if the bladder is capacious and arousal intact, and will wet only if a second system also fails.

The power of the model is that it maps directly onto treatment. Overproduction of urine, nocturnal polyuria, is the target of desmopressin, which replaces the missing hormonal signal to concentrate the night-time urine. A small or overactive bladder, reduced nocturnal bladder capacity, is the target of bladder-directed measures and, where there is daytime overactivity, anticholinergic medication. The failure to wake, a high arousal threshold, is the target of the enuresis alarm, which trains the sleeping child to respond to the bladder signal (Nevéus, 2017). Because the three systems are dissociable, two children with identical wet nights may need entirely different treatments, and the clinician's task is to work out which system, or combination, is driving a given child's bedwetting.

Pathophysiology: Urine, Bladder, and Arousal

The best-understood system is the renal one. In healthy people the pituitary releases more antidiuretic hormone, vasopressin, at night, so that the kidneys concentrate the urine and far less is produced during sleep than during the day. The landmark observation of the field is that many children with nocturnal enuresis lack this nocturnal rise: their plasma vasopressin does not climb at night, so their kidneys go on producing dilute urine around the clock, and the night-time volume can exceed what the bladder can hold (Rittig et al., 1989). This absent circadian rhythm of vasopressin is the physiological basis of nocturnal polyuria and the rationale for desmopressin, a synthetic vasopressin analogue.

The second system is the bladder. Some children have a reduced functional capacity at night, or a detrusor that contracts uninhibitedly during sleep, so that even a normal volume of urine triggers emptying before morning; this pattern tends to track with daytime overactivity and so with the non-monosymptomatic form. The third system is arousal. Children who wet at night are, as a group, difficult to wake, and the modern synthesis places a high arousal threshold at the centre of the disorder: the bladder signal that would wake most people fails to rouse the enuretic child, so the reflex to void proceeds without waking (Nevéus, 2017). The current understanding links this to brainstem arousal circuitry and frames enuresis as, in part, a disorder of sleep arousal rather than of the bladder alone, which is why a treatment that teaches arousal, the alarm, is so effective.

The Cognitive and Behavioural Dimension

What makes bedwetting a topic for cognitive psychology, and not only for paediatric nephrology, is that its central treatment is a learning procedure and its central comorbidities are disorders of attention and self-regulation. The enuresis alarm works by classical conditioning: it pairs the sensation of a full or emptying bladder with an arousing stimulus until the child learns to wake, or to inhibit voiding, in response to the bladder signal alone. Staying dry at night, in other words, can be trained, which places the condition squarely in the behavioural domain.

The comorbidity with attention-deficit/hyperactivity disorder is the clearest cognitive link. Children with nocturnal enuresis have elevated rates of ADHD, and the overlap matters for treatment because the alarm is a demanding routine that requires sustained attention and adherence over weeks, exactly what an inattentive child finds hardest (von Gontard & Equit, 2015). More broadly, incontinence of all kinds carries a real burden of psychological and psychiatric comorbidity that is not merely a reaction to the wetting but part of a shared substrate of self-regulation and neurodevelopment (von Gontard et al., 2011). This is why contemporary guidelines assess behaviour and attention alongside the bladder and the fluid chart, and why the distress of bedwetting, its effect on self-esteem and on the child's social life, is treated as part of the condition rather than a side issue (von Gontard & Kuwertz-Bröking, 2019).

Epidemiology

Nocturnal enuresis is common in early school age and becomes less so each year as the systems mature. Around one in six or seven children wet the bed at age five, and the prevalence falls steadily through childhood, so that by adolescence only one or two per cent are affected; it is more common in boys than in girls, the reverse of the sex ratio for daytime wetting (Robson, 2009). The large British ALSPAC birth-cohort study mapped this decline in detail, distinguishing infrequent bedwetting from the more persistent form and giving the age-by-age frequencies that anchor the modern figures (Butler & Heron, 2008). Bedwetting also runs strongly in families: a child with an affected parent is markedly more likely to be enuretic, and the condition shows a clear hereditary pattern, which fits the account of it as a delay in the maturation of the very systems, vasopressin rhythm, bladder, and arousal, that normally bring night-time dryness (Robson, 2009; Nevéus, 2017).

The key epidemiological fact is the high rate of spontaneous resolution: roughly fifteen per cent of children who wet the bed become dry each year without any treatment, as the nocturnal vasopressin rhythm matures, the bladder grows, and the arousal system develops. This is why the decision to treat weighs the child's distress and the family's burden, not the wetting alone, and why watchful waiting is a legitimate option for a young child who is not troubled by it. It is also why treatment trials must be read against a high background resolution rate, and why a durable cure, rather than mere suppression of symptoms while on medication, is the standard against which treatments are judged.

Assessment and Treatment

Assessment is built to separate the straightforward monosymptomatic case from the non-monosymptomatic one and to identify which systems are at fault, because that dictates the treatment. The core tools are simple and behavioural: a history that asks specifically about daytime symptoms, a frequency-volume chart that records daytime voided volumes, and a night-time record of wet nights and of the volume of urine produced overnight, which together reveal whether the child has nocturnal polyuria, a small bladder, or both. A urinalysis excludes infection and diabetes, and constipation is sought and treated because it reduces bladder capacity (Vande Walle et al., 2012).

The two first-line treatments follow from the three-system model. The enuresis alarm, a moisture sensor that sounds when the child begins to wet, is a conditioning therapy, and the Cochrane systematic review establishes it as the intervention with the most durable effect: about two-thirds of children become dry during treatment and many stay dry afterwards, because the alarm trains a lasting response rather than suppressing a symptom (Glazener et al., 2005). Desmopressin, the synthetic vasopressin analogue, works faster and is well suited to the child with nocturnal polyuria and a normal bladder capacity, but its effect is largely confined to the nights it is taken, so relapse on stopping is common (Nevéus et al., 2020). The management standard sets these two as first-line and reserves anticholinergics, for a small or overactive bladder, and combination regimens for children who do not respond to either alone (Nevéus et al., 2020). The choice between alarm and desmopressin is itself guided by the model: polyuria points to desmopressin, a small bladder or a need for a lasting cure points to the alarm.

Figure

Figure 1

Why a Child Wets: Night Urine Volume Against Bladder Capacity

Two overnight urine-production traces against a bladder-capacity line: a normal child stays below capacity, an enuretic child with nocturnal polyuria crosses it before morning A line graph of cumulative overnight urine volume against hours of sleep. A horizontal line marks nocturnal bladder capacity. The lower trace, a child with a normal vasopressin rise, rises slowly and stays below the capacity line until morning. The upper trace, a child with nocturnal polyuria, rises steeply and crosses the capacity line partway through the night, at which point a wet episode is marked. a wet night is urine output outrunning bladder capacity cumulative urine (mL) hours of sleep nocturnal bladder capacity normal vasopressin rise: stays below capacity nocturnal polyuria: crosses capacity wet episode
Note. A wet night occurs when overnight urine output exceeds the bladder's night-time capacity before the child wakes. With a normal nocturnal vasopressin rise (green) urine accumulates slowly and stays below capacity until morning. In nocturnal polyuria (blue) the absent vasopressin rise lets urine accumulate quickly, crossing the capacity line (red) partway through the night; if arousal fails, a wet episode follows. Schematic, not measured data. Original schematic after the framework of Butler and Holland (2000) and Rittig et al. (1989).

Interactive Demonstrations

The three demonstrations below make the core ideas manipulable. The first is a night-profile simulator: adjust the nocturnal urine output, the bladder's night-time capacity, and the arousal threshold, and watch whether the child stays dry, wakes in time, or wets the bed. The second is a three-system classifier that takes a child's profile and names the dominant failing system and the treatment it points to. The third is an alarm-conditioning curve that shows how the probability of a dry night rises over weeks of alarm training and how relapse differs between the alarm and desmopressin.

Demo 1 — The night-profile simulator

A wet night is three systems interacting, not one failing. Set the child’s overnight urine output, the bladder’s night-time capacity, and how deeply the child sleeps (the arousal threshold). Urine accumulates across the night; if it reaches capacity before morning the bladder signals. A light sleeper wakes in time and stays dry; a deep sleeper sleeps through the signal and wets.

360 mL overnight
240 mL
very deep sleeper
capacity 240 mLasleepmorningcumulative urine
cumulative urine bladder capacity

Wet night. Output of 360 mL crosses the 240 mL capacity partway through the night, and a very deep sleeper fails to wake — the void reflex proceeds asleep. The volume mismatch plus the high arousal threshold together produce the wet bed.

The three-system model as a single trace: urine output against bladder capacity, with arousal deciding whether a crossing wakes the child or wets the bed. Computed locally from the controls, deterministic, not stored.

Demo 2 — The three-system classifier

The failing system dictates the treatment, and it is read from the child’s profile. Set how marked each of the three systems is — nocturnal polyuria (overnight urine excess), reduced bladder capacity, and a high arousal threshold — and the classifier names the dominant system and the treatment the three-system model points to.

marked
absent
mild
polyuriasmall bladderarousal

Dominant system: Nocturnal polyuria — a blunted nocturnal vasopressin rise lets the kidneys overproduce urine at night, beyond what the bladder can store. Treatment it points to: desmopressin, which replaces the missing hormonal signal to concentrate the night-time urine.

A fixed decision rule over three systems, not a diagnostic instrument: polyuria points to desmopressin, a small bladder to bladder-directed measures, a high arousal threshold to the alarm. Computed locally, deterministic, not stored.

Demo 3 — Alarm conditioning versus desmopressin

The two first-line treatments differ not in peak effect but in what they leave behind. Drag the week to watch the dry-night rate for each. The alarm is a conditioning therapy: its effect builds over weeks and is largely retained after it stops. Desmopressin acts at once but mainly on the nights it is taken, so the gain relapses when it is withdrawn. Treatment runs for 8 weeks, then stops.

week 12 — after treatment stopped
treatment stopsweek 0week 16dry-night rate
enuresis alarm (conditioning) desmopressin (suppression)

At week 12 (after treatment stopped), the alarm gives a dry-night rate of 72% and desmopressin 34%. After treatment stops, the alarm’s learned response largely holds while desmopressin relapses toward the untreated baseline — the durability difference the Cochrane evidence describes.

A schematic of durability, not trial data: conditioning (alarm) is retained after withdrawal, suppression (desmopressin) is not. Curves computed locally from fixed functions, deterministic, not stored.

Worked Example

Consider how a clinician decides whether a child's bedwetting is driven by nocturnal polyuria, the question that points toward desmopressin. The reasoning rests on two numbers: how much urine the child produces overnight, and how much the bladder can be expected to hold. Expected bladder capacity in children is estimated by the International Children's Continence Society formula: capacity in millilitres equals thirty times the quantity age-in-years plus one. For a seven-year-old this gives thirty times eight, which is two hundred and forty millilitres.

Nocturnal polyuria is then defined as an overnight urine production, the volume in the morning-emptied nappy or first morning void plus any night-time voids, that exceeds one hundred and thirty per cent of expected bladder capacity. For our seven-year-old, one hundred and thirty per cent of two hundred and forty millilitres is three hundred and twelve millilitres. Suppose the family's night record shows an overnight production of three hundred and sixty millilitres. That is one hundred and fifty per cent of expected capacity, above the three-hundred-and-twelve-millilitre threshold, so the child has nocturnal polyuria.

The worked lesson is that two simple measurements turn a complaint into a mechanism and a treatment. An overnight volume of three hundred and sixty millilitres means little on its own, but set against an age-expected capacity of two hundred and forty it places the child firmly in the nocturnal-polyuria group, whose wetting reflects a renal, hormonal problem rather than a small bladder, and points first-line treatment toward desmopressin, which supplies the missing night-time vasopressin, rather than toward the alarm alone (Nevéus et al., 2020; Vande Walle et al., 2012).

Discussion

Nocturnal enuresis sits at the join of several disciplines. It is a renal and endocrine sign, the output of a kidney that is not concentrating the night-time urine because the hormone that should tell it to is not rising; it is a urological one, bound up with the capacity and stability of the bladder; and it is a behavioural and neurological one, a disorder of arousal from sleep whose central cure is a conditioning procedure. The history of the field is the story of integrating these: the three-system model gave a single framework in which renal, bladder, and arousal failures could be weighed against one another, and the discovery of the absent nocturnal vasopressin rhythm gave the renal arm a concrete mechanism and a rational drug.

The unifying theme is that bedwetting is usually a developmental mismatch rather than a disease, which is why spontaneous resolution is so common and why the best treatment, the alarm, works by accelerating the very learning that time would otherwise bring. The comorbidities make the same point from the other side: the overlap with attention-deficit/hyperactivity disorder ties the condition to the broader development of self-regulation, and the stress that can precipitate secondary enuresis ties it to the child's emotional life. The open problems are those of prediction and adherence, which child will respond to the alarm and which to desmopressin, and how to sustain a demanding nightly routine in the children, many of them inattentive, who find routines hardest to keep.

Current Directions

The most active front is the refinement of the pathophysiological account and its translation into better-targeted treatment. The modern synthesis of enuresis pathogenesis has shifted the centre of gravity toward the brain, framing the condition as a disorder of sleep arousal and brainstem function in which the bladder and the kidney are contributing systems rather than the whole story (Nevéus, 2017). The direction of travel is toward matching treatment to the dominant failing system identified at assessment, rather than trying each therapy in turn.

A second direction is the consolidation of management into clear, evidence-based pathways. The International Children's Continence Society's updated management standard set out the current treatment hierarchy and the order in which the alarm, desmopressin, and second-line agents should be considered (Nevéus et al., 2020), and national guideline reviews have translated this into practical diagnostic and treatment algorithms for the general clinician, emphasising the frequency-volume chart and the monosymptomatic/non-monosymptomatic split as the pivotal early decisions (von Gontard & Kuwertz-Bröking, 2019). The emphasis throughout is on treating the right system in the right order, and on measuring durable dryness rather than symptom suppression as the mark of success.

Common Misconceptions

Bedwetting means the child is lazy or could stop if they tried.
Nocturnal enuresis is an involuntary event during sleep, driven by overnight urine output, bladder capacity, and a high arousal threshold, not by will; the child is asleep and cannot choose to stop it (Butler & Holland, 2000; Nevéus, 2017).
It is the same thing as daytime wetting.
Night-time and daytime wetting are distinct signs with different mechanisms; the International Children's Continence Society reserves enuresis for sleep wetting, and the presence of daytime symptoms defines the non-monosymptomatic form that must be treated differently (Austin et al., 2016; Nevéus et al., 2010).
Bedwetting is caused by drinking too much before bed.
The usual cause is a blunted nocturnal rise in vasopressin, so the kidneys overproduce urine at night regardless of evening drinking; fluid timing is a minor factor beside the underlying hormonal and arousal problem (Rittig et al., 1989).
Medication is the best first treatment.
The enuresis alarm, a conditioning therapy, has the most durable effect, with many children staying dry after treatment ends, whereas desmopressin mainly works on the nights it is taken; the choice depends on the child's profile, not on a general preference for a pill (Glazener et al., 2005; Nevéus et al., 2020).

Glossary

Alarm therapy.
A conditioning treatment in which a moisture sensor sounds as the child begins to wet, training the sleeping child to wake to, or inhibit, a full bladder; the treatment with the most durable effect.
Arousal threshold.
The strength of stimulus needed to wake a sleeper; a high threshold, so that the bladder signal fails to rouse the child, is central to the modern account of enuresis.
Desmopressin.
A synthetic analogue of vasopressin given to replace the absent nocturnal rise in the hormone, concentrating the night-time urine; first-line for nocturnal polyuria.
Detrusor overactivity.
Involuntary contractions of the bladder muscle during filling; when present at night it reduces functional capacity and contributes to the non-monosymptomatic form.
Enuresis.
Involuntary urination in a child past the age of expected control; in current ICCS usage, specifically wetting during sleep.
Expected bladder capacity.
The age-predicted bladder volume, estimated as thirty times (age in years plus one) millilitres; the yardstick against which overnight urine output is judged.
Monosymptomatic nocturnal enuresis.
Bedwetting with no daytime lower-urinary-tract symptoms; the straightforward form that responds well to the alarm or desmopressin.
Nocturnal enuresis.
Involuntary urination during sleep in a child past the age of expected bladder control; the clinical term for bedwetting.
Nocturnal polyuria.
An overnight urine output exceeding about 130% of expected bladder capacity, usually from a blunted nocturnal vasopressin rise; the target of desmopressin.
Non-monosymptomatic nocturnal enuresis.
Bedwetting accompanied by daytime bladder symptoms such as urgency or incontinence; the daytime problem must be treated before the night-time wetting.
Primary nocturnal enuresis.
Bedwetting in a child who has never had a sustained dry period of six months; the common, usually developmental form.
Reduced nocturnal bladder capacity.
A night-time functional bladder volume smaller than expected for age, so that even a normal urine output triggers emptying before morning.
Secondary nocturnal enuresis.
Bedwetting that returns after at least six months of dryness; prompts a search for a precipitant such as stress, infection, or new illness.
Three-systems model.
The framework that explains bedwetting as the interaction of nocturnal urine output, bladder capacity, and arousal from sleep, any of which can tip a child into wetting.
Vasopressin.
The antidiuretic hormone whose normal nocturnal rise concentrates the night-time urine; its absent rhythm is the basis of nocturnal polyuria.
Voiding diary.
A frequency-volume chart of daytime voided volumes and overnight urine output; the central tool for classifying the enuresis and identifying the failing system.

Key Researchers

Alexander von Gontard

(formerly Saarland University). Child and adolescent psychiatrist whose work established the psychiatric comorbidity of incontinence, the ADHD and behavioural associations that make nocturnal enuresis a cognitive-behavioural as well as a physiological condition. ORCID · Wikidata

Tryggve Nevéus

(Uppsala University). Paediatric nephrologist and former President of the International Children's Continence Society; lead author of the ICCS standardization and management documents and of the modern synthesis of enuresis pathogenesis. ORCID · Faculty

Søren Rittig

(Aarhus University). Paediatrician whose landmark work established the absent nocturnal rise in vasopressin that produces nocturnal polyuria, the physiological mechanism at the centre of the three-system model. ORCID · Faculty · Scholar

Johan Vande Walle

(Ghent University Hospital). Paediatric nephrologist whose work on desmopressin and nocturnal polyuria underpins the pharmacological arm of enuresis treatment and the practical consensus guidelines for management. ORCID

Frequently Asked Questions

What is nocturnal enuresis?

It is involuntary urination during sleep in a child who is past the age of expected night-time bladder control, conventionally five years. It is the clinical name for bedwetting.

What causes bedwetting?

Most cases arise from a mismatch between three systems: the kidneys produce too much urine overnight, usually because the normal night-time rise in the hormone vasopressin is blunted; the bladder holds too little; and the child sleeps too deeply to wake to the bladder signal. A given child may have a problem in one, two, or all three.

How is it different from daytime wetting?

Nocturnal enuresis happens during sleep; daytime incontinence happens while the child is awake. They have different mechanisms and different treatments, and when both are present the daytime problem is treated first.

What is the difference between primary and secondary bedwetting?

Primary enuresis means the child has never had a long dry spell and is usually developmental. Secondary enuresis means wetting has returned after at least six months of dryness, which prompts a search for a trigger such as stress, a urinary infection, constipation, or new illness.

Does an enuresis alarm work?

Yes. The alarm is a conditioning treatment that trains the child to wake to a full bladder, and it has the most durable effect of any treatment: about two-thirds of children become dry during treatment and many stay dry afterwards. It requires several weeks of consistent use.

What is desmopressin and when is it used?

Desmopressin is a synthetic form of the hormone vasopressin that reduces overnight urine production. It suits children with nocturnal polyuria and a normal bladder, works quickly, and is useful for short-term needs such as sleepovers, but wetting often returns when it is stopped.

Is bedwetting linked to ADHD?

Yes. Children with nocturnal enuresis have elevated rates of attention-deficit/hyperactivity disorder, which also makes the demanding alarm routine harder to sustain, so attention and behaviour are assessed alongside the bladder.

Will a child grow out of it?

Usually. About fifteen per cent of bedwetting children become dry each year on their own as the systems mature, so spontaneous resolution is common. Treatment is offered when the wetting distresses the child or burdens the family, rather than for the wetting alone.

References

Austin, P. F., Bauer, S. B., Bower, W., Chase, J., Franco, I., Hoebeke, P., ... Nevéus, T. (2016). The standardization of terminology of lower urinary tract function in children and adolescents: Update report from the Standardization Committee of the International Children's Continence Society. Neurourology and Urodynamics, 35(4), 471–481. https://doi.org/10.1002/nau.22751

Butler, R. J., & Heron, J. (2008). The prevalence of infrequent bedwetting and nocturnal enuresis in childhood: A large British cohort. Scandinavian Journal of Urology and Nephrology, 42(3), 257–264. https://doi.org/10.1080/00365590701748054

Butler, R. J., & Holland, P. (2000). The three systems: A conceptual way of understanding nocturnal enuresis. Scandinavian Journal of Urology and Nephrology, 34(4), 270–277. https://doi.org/10.1080/003655900750042022

Glazener, C. M. A., Evans, J. H. C., & Peto, R. E. (2005). Alarm interventions for nocturnal enuresis in children. Cochrane Database of Systematic Reviews, (2), CD002911. https://doi.org/10.1002/14651858.CD002911.pub2

Nevéus, T., Eggert, P., Evans, J., Macedo, A., Rittig, S., Tekgül, S., ... Robson, L. (2010). Evaluation of and treatment for monosymptomatic enuresis: A standardization document from the International Children's Continence Society. The Journal of Urology, 183(2), 441–447. https://doi.org/10.1016/j.juro.2009.10.043

Nevéus, T. (2017). Pathogenesis of enuresis: Towards a new understanding. International Journal of Urology, 24(3), 174–182. https://doi.org/10.1111/iju.13310

Nevéus, T., von Gontard, A., Hoebeke, P., Hjälmås, K., Bauer, S., Bower, W., ... Djurhuus, J. C. (2006). The standardization of terminology of lower urinary tract function in children and adolescents: Report from the Standardisation Committee of the International Children's Continence Society. The Journal of Urology, 176(1), 314–324. https://doi.org/10.1016/S0022-5347(06)00305-3

Nevéus, T., Fonseca, E., Franco, I., Kawauchi, A., Kovacevic, L., Nieuwhof-Leppink, A., ... Rittig, S. (2020). Management and treatment of nocturnal enuresis—an updated standardization document from the International Children's Continence Society. Journal of Pediatric Urology, 16(1), 10–19. https://doi.org/10.1016/j.jpurol.2019.12.020

Rittig, S., Knudsen, U. B., Nørgaard, J. P., Pedersen, E. B., & Djurhuus, J. C. (1989). Abnormal diurnal rhythm of plasma vasopressin and urinary output in patients with enuresis. The American Journal of Physiology, 256(4 Pt 2), F664–F671. https://doi.org/10.1152/ajprenal.1989.256.4.F664

Robson, W. L. M. (2009). Evaluation and management of enuresis. The New England Journal of Medicine, 360(14), 1429–1436. https://doi.org/10.1056/NEJMcp0808009

Vande Walle, J., Rittig, S., Bauer, S., Eggert, P., Marschall-Kehrel, D., & Tekgül, S. (2012). Practical consensus guidelines for the management of enuresis. European Journal of Pediatrics, 171(6), 971–983. https://doi.org/10.1007/s00431-012-1687-7

von Gontard, A., & Equit, M. (2015). Comorbidity of ADHD and incontinence in children. European Child & Adolescent Psychiatry, 24(2), 127–140. https://doi.org/10.1007/s00787-014-0577-0

von Gontard, A., Baeyens, D., Van Hoecke, E., Warzak, W. J., & Bachmann, C. (2011). Psychological and psychiatric issues in urinary and fecal incontinence. The Journal of Urology, 185(4), 1432–1436. https://doi.org/10.1016/j.juro.2010.11.051

von Gontard, A., & Kuwertz-Bröking, E. (2019). The diagnosis and treatment of enuresis and functional daytime urinary incontinence. Deutsches Ärzteblatt International, 116(16), 279–285. https://doi.org/10.3238/arztebl.2019.0279