Objective. The most effective nonpharmacological treatment for insomnia disorder is cognitive behavioural therapy-insomnia (CBT-i). However CBT-i may not suit everyone. Auricular acupuncture (AA) is a complementary treatment. Studies show that it may alleviate insomnia symptoms. The aim of this randomised controlled study was to compare treatment effects of AA with CBT-i and evaluate symptoms of insomnia severity, anxiety, and depression. Method. Fifty-nine participants, mean age 60.5 years (SD 9.4), with insomnia disorder were randomised to group treatment with AA or CBT-i. Self-report questionnaires, the Insomnia Severity Index (ISI), Dysfunctional Beliefs and Attitudes about Sleep scale (DBAS-16), Epworth Sleepiness Scale (ESS), and Hospital Anxiety and Depression scale (HAD), were collected at baseline, after treatment, and at 6-month follow-up. A series of linear mixed models were performed to examine treatment effect over time between and within the groups. Results. Significant between-group improvements were seen in favour of CBT-i in ISI after treatment and at the 6-month follow-up and in DBAS-16 after treatment. Both groups showed significant within-group postintervention improvements in ISI, and these changes were maintained six months later. The CBT-i group also showed a significant reduction in DBAS-16 after treatment and six months later. Conclusions. Compared to CBT-i, AA, as offered in this study, cannot be considered an effective stand-alone treatment for insomnia disorder.

Introduction: The interest in non-pharmacological interventions for insomnia disorder has increased. The aim was to assess the immediate treatment effects of auricular acupuncture (AA) and cognitive behavioural therapy for insomnia (CBT-i) regarding discontinuation of hypnotic usage and symptoms of anxiety, depression and insomnia.

Method: Prospective randomised controlled study. Fifty-seven participants (mean age 61 years (SD 8.6)) with insomnia disorder and long-term use of non-benzodiazepine hypnotics received group-treatment with AA or CBT-i. Pre- and post-treatment measures included symptoms of anxiety, depression and insomnia via self-report questionnaires: Hospital Anxiety and Depression scale (HAD-A, HAD-D) and Insomnia Severity Index (ISI). Other sleep parameters and hypnotic consumption were measured with a sleep diary. Linear mixed models were performed to examine treatment effect over time within and between the groups.

Results: Seventy-one percent of the AA participants and 84% of the CBT-i participants managed to discontinue their hypnotic drug consumption post-treatment. Symptoms of anxiety and depression decreased within the AA group (HAD-A (p < 0.05), HAD-D (p < 0.05)) and insomnia symptoms decreased within the CBT-i group (ISI (p < 0.001)). The only between-group difference occurred in ISI (p < 0.001), in favour of CBT-i. According to the within-group sleep diary results, the CBT-i group went to bed later (p < 0.001), fell asleep quicker (p < 0.05), increased their sleep efficiency (p < 0.001) and self-rated sleep quality (p < 0.05) post-treatment.

Conclusions: Both groups ended/maintained low hypnotic drug consumption post-treatment. Short-term reductions occurred in the AA group in anxiety and depression symptoms and in the CBT-i group regarding insomnia symptoms.

The aim of the study was to objectively examine how sleep patterns were affected in a short- and long-term perspective after auricular acupuncture (AA) and cognitive behavioral therapy for insomnia (CBT-i). Sixty participants with insomnia disorders (men/women 9/51; mean age of 60.5 years, (SD 9.4)), were randomized to group treatment with AA or CBT-i. Actigraphy recordings were made at baseline, post-treatment and 6-month follow-up. The CBT-i group reduced their time in bed, their actual sleeping time, their sleep latency and their actual time awake. The AA group slept longer, increased their time in bed and decreased their sleep latency post-treatment. The between-groups results differed in wake-up time, rising, time in bed, actual sleep time and actual wake time. The differences were not maintained six months later. In accordance with previous findings the results support the notion that the objective sleep time does not necessarily affect the subjective perception of insomnia.

Delayed sleep phase disorder (DSPD) is common among young people, but there is still no evidence-based treatment available. In the present study, the feasibility of cognitive behavioral therapy (CBT) was evaluated as an additive treatment to light therapy (LT) in DSPD. A randomized controlled trial with participants aged 16 to 26 years received LT for two weeks followed by either four weeks of CBT or no treatment (NT). LT advanced sleep-wake rhythm in both groups. Comparing LT+CBT with LT+NT, no significant group differences were observed in the primary endpoints. Although anxiety and depression scores were low at pretreatment, they decreased significantly more in LT+CBT compared to LT+NT. The results are discussed and some suggestions are given for further studies.

Clinical trials with light therapy (LT) for delayed sleep phase disorder (DSPD) are sparse and little is known about factors that are favorable for improvements. In this study, LT with scheduled rise times was conducted at home for 14 days by 44 participants with DSPD aged 16–26 years. Primary outcomes were sleep onset and sleep offset. Potential predictors were demographic characteristics, chronotype, dim light melatonin onset, the number of days the LT lamp was used, the daily duration of LT, daytime sleepiness, anxiety, depression, worry, and rumination. Significant advances were observed in sleep onset and sleep offset from baseline to the end of treatment. The number of days of LT predicted earlier sleep onset and sleep offset.

During puberty, there is a known delay in sleep–wake preference and circadian rhythm (Carskadon, Acebo, & Jenni, 2004Carskadon, M. A., Acebo, C., & Jenni, O. G. (2004). Regulation of adolescent sleep: Implications for behavior. Annals of the New York Academy of Sciences, 1021, 276–291.; Carskadon, Vieira, & Acebo, 1993 Carskadon, M. A., Vieira, C., & Acebo, C. (1993). Association between puberty and delayed phase preference. Sleep, 16, 258–262.). If this delay becomes persistent and causes a functional impairment, the person has developed delayed sleep phase disorder (DSPD). DSPD is most common among adolescents and young adults, and the prevalence is about 1–10% in this group (American Academy of Sleep Medicine, 2014 American Academy of Sleep Medicine. (2014). International classification of sleep disorders. Diagnostic and coding manual (3d ed.). Westchester, IL: Author.; Lovato, Gradisar, Short, Dohnt, & Micic, 2013 Lovato, N., Gradisar, M., Short, M., Dohnt, H., & Micic, G. (2013). Delayed sleep phase disorder in an Australian school-based sample of adolescents. Journal of Clinical Sleep Medicine, 9, 939–944.; Weitzman et al., 1981 Weitzman, E. D., Czeisler, C. A., Coleman, R. M., Spielman, A. J., Zimmerman, J. C., Dement, W.,… Pollak, C. P. (1981). Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia. Archives of General Psychiatry, 38, 737–746.). This disorder often includes difficulties initiating sleep, fatigue, daytime sleepiness, concentration difficulties, irritability, depressive symptoms, and anxiety. Social consequences often related to DSPD are truancy, late arrival to school or work, substance abuse, and poor academic performance (Barion & Zee, 2007 Barion, A., & Zee, P. C. (2007). A clinical approach to circadian rhythm sleep disorders. Sleep Medicine, 8, 566–577.; Dagan, Stein, Steinbock, Yovel, & Hallis, 1998 Dagan, Y., Stein, D., Steinbock, M., Yovel, I., & Hallis, D. (1998). Frequency of delayed sleep phase syndrome among hospitalized adolescent psychiatric patients. Journal of Psychosomatic Research, 45, 15–20.; Dewald, Meijer, Oort, Kerkhof, & Bogels, 2010 Dewald, J. F., Meijer, A. M., Oort, F. J., Kerkhof, G. A., & Bogels, S. M. (2010). The influence of sleep quality, sleep duration and sleepiness on school performance in children and adolescents: A meta-analytic review. Sleep Medicine Reviews, 14, 179–189.; Lovato et al., 2013 Lovato, N., Gradisar, M., Short, M., Dohnt, H., & Micic, G. (2013). Delayed sleep phase disorder in an Australian school-based sample of adolescents. Journal of Clinical Sleep Medicine, 9, 939–944.; Ohta, Iwata, Kayukawa, & Okada, 1992 Ohta, T., Iwata, T., Kayukawa, Y., & Okada, T. (1992). Daily activity and persistent sleep-wake schedule disorders. Progress in Neuropsychopharmacology and Biological Psychiatry, 16, 529–537.; Saxvig, Pallesen, Wilhelmsen-Langeland, Molde, & Bjorvatn, 2012 Saxvig, I. W., Pallesen, S., Wilhelmsen-Langeland, A., Molde, H., & Bjorvatn, B. (2012). Prevalence and correlates of delayed sleep phase in high school students. Sleep Med, 13(2), 193–199.; Sivertsen, Harvey, Pallesen, & Hysing, 2015 Sivertsen, B., Harvey, A. G., Pallesen, S., & Hysing, M. (2015). Mental health problems in adolescents with delayed sleep phase: Results from a large population-based study in Norway. Journal of Sleep Research, 24, 11–18.; Sivertsen et al., 2013 Sivertsen, B., Pallesen, S., Stormark, K. M., Boe, T., Lundervold., A. E., & Hysing, M. (2013). Delayed sleep phase syndrome in adolescents: Prevalence and correlates in a large population based study. BMC Public Health, 13, 1663.; Sivertsen, Glozier, Harvey, & Hysing, 2015 Sivertsen, B., Glozier, N., Harvey, A. G., & Hysing, M. (2015). Academic performance in adolescents with delayed sleep phase. Sleep Medicine, 16, 1084–1090.; Thorpy, Korman, Spielman, & Glovinsky, 1988 Thorpy, M. J., Korman, E., Spielman, A. J., & Glovinsky, P. B. (1988). Delayed sleep phase syndrome in adolescents. Journal of Adolescent Health Care, 9, 22–27.).

Despite the distress and dysfunction caused by DSPD, motivation to start treatment and compliance to treatment are often problematic among persons with DSPD (Barion & Zee, 2007Barion, A., & Zee, P. C. (2007). A clinical approach to circadian rhythm sleep disorders. Sleep Medicine, 8, 566–577.). Bright light exposure in the morning is one of the recommended treatments for DSPD (Morgenthaler et al., 2007 Morgenthaler, T. I., Lee-Chiong, T., Alessi, C., Friedman, L., Aurora, R. N., Boehlecke, B.,… Zac, R. (2007). Standards of Practice Committee of the American Academy of Sleep Medicine: Practice parameters for the clinical evaluation and treatment of circadian rhythm sleep disorders [American Academy of Sleep Medicine report]. Sleep, 30, 1445–1459.). To date, there are no evidence-based guidelines for the duration of each LT session, the duration of the total treatment, the intensity of the lamp, or the exact timing in the morning of LT. In clinical practice, LT with bright white light for 30–45 min every morning is often recommended for patients with DSPD (Bjorvatn & Pallesen, 2009 Bjorvatn, B., & Pallesen, S. (2009). A practical approach to circadian rhythm sleep disorders. Sleep Medicine Reviews, 13, 47–60.). For optimal effect, LT in the morning should be combined with dim light in the evening (Hoban & Sulzman, 1985 Hoban, T. M., & Sulzman, F. M. (1985). Light effects on circadian timing system of a diurnal primate, the squirrel monkey. American Journal of Physiology, 249(2), R274–R280.; Rosenthal et al., 1990 Rosenthal, N. E., Joseph-Vanderpool, J. R., Levendosky, A. A., Johnston, S. H., Allen, R., Kelly, K. A.,… Starz, K. E. (1990). Phase-shifting effects of bright morning light as treatment for delayed sleep phase syndrome. Sleep, 13, 354–361.). LT is a safe treatment with only a few side effects that are generally mild and short-lived (Kogan & Guilford, 1998 Kogan, A. O., & Guilford, P. M. (1998). Side effects of short-term 10,000-lux light therapy. American Journal of Psychiatry, 155, 293–294.).

Most studies on the phase-advancing effects of LT on the circadian rhythm have been conducted in healthy subjects under strict laboratory conditions and focused on internal phase markers. These studies demonstrate that the circadian rhythm is affected by light through a phase-response curve. Light before the temperature nadir delays the circadian rhythm, and light after the temperature nadir advances the circadian rhythm (Boivin, Duffy, Kronauer, & Czeisler, 1996Boivin, D. B., Duffy, J. F., Kronauer, R. E., & Czeisler, C. A. (1996). Dose-response relationships for resetting of human circadian clock by light. Nature, 379(6565), 540–542.; Dewan, Benloucif, Reid, Wolfe, & Zee, 2011 Dewan, K., Benloucif, S., Reid, K., Wolfe, L. F., & Zee, P. C. (2011). Light-induced changes of the circadian clock of humans: Increasing duration is more effective than increasing light intensity. Sleep, 34, 593–599.; Khalsa, Jewett, Cajochen, & Czeisler, 2003 Khalsa, S. B., Jewett, M. E., Cajochen, C., & Czeisler, C. A. (2003). A phase response curve to single bright light pulses in human subjects. Journal of Physiology, 549(3), 945–952.; Minors, Waterhouse, & Wirz-Justice, 1991 Minors, D. S., Waterhouse, J. M., & Wirz-Justice, A. (1991). A human phase-response curve to light. Neuroscience Letter, 133, 36–40.; Revell, Molina, & Eastman, 2012 Revell, V. L., Molina, T. A., & Eastman, C. I. (2012). Human phase respose curve to intermittent blue light using a commercially available device. Journal of Physiology, 590(19), 4859–4868.). Bright light (10,000 lux) in a self-administered format has, in a randomized controlled trial, been shown to advance temperature nadir and decreases daytime sleepiness for persons with DSPD (Rosenthal et al., 1990 Rosenthal, N. E., Joseph-Vanderpool, J. R., Levendosky, A. A., Johnston, S. H., Allen, R., Kelly, K. A.,… Starz, K. E. (1990). Phase-shifting effects of bright morning light as treatment for delayed sleep phase syndrome. Sleep, 13, 354–361.). However, a recent study demonstrated that gradually advanced wake-up times combined with bright light (10,000 lux) did not have significantly better effect than gradually advanced wake-up times combined with orange light (400 lux) on sleep diary data and dim light melatonin onset (DLMO) in DSPD (Saxvig et al., 2014 Saxvig, I. W., Wilhelmsen-Langeland, A., Pallesen, S., Vedaa, O., Nordhus, I. H., & Bjorvatn, B. (2014). A randomized controlled trial with bright light and melatonin for delayed sleep phase disorder: Effects on subjective and objective sleep. Chronobiology International, 31, 72–86.).

The aim of the present study was to investigate the effect of self-administered LT with scheduled rise times on the sleep-wake rhythm and daytime functioning. In this study, we also wanted to examine possible predictors of the outcome. To our knowledge, predictors of the effect of scheduled LT in patients with DSPD have so far not been investigated. Daytime sleepiness, anxiety, and depression were investigated as predictors since they are common symptoms in DSPD. Worry and rumination were investigated as possible predictors as they are common clinical features in persons with sleep difficulties (Carney, Harris, Falco, & Edinger, 2013Carney, C. E., Harris, A. L., Falco, A., & Edinger, J. D. (2013). The relation between insomnia symptoms, mood, and rumination about insomnia symptoms. Journal of Clinical Sleep Medicine, 9, 567–575.; Carney, Harris, Moss, & Edinger, 2010 Carney, C. E., Harris, A. L., Moss, T. G., & Edinger, J. D., (2010). Distinguishing rumination from worry in clinical insomnia. Behavioral Research Therapy, 48, 540–546.). Since little is known about how LT should be administered at home, the number of days the LT lamp was used and the daily duration of LT were investigated as possible predictors. Time of DLMO and chronotype preference was investigated as possible predictors since they are measures of the delay in diurnal rhythm. Understanding predicting factors can be important to identify persons with DSPD that might need extra support during LT, and to isolate factors during LT that can improve the treatment response.

A delayed sleep-wake and circadian rhythm often occurs during puberty. While some individuals only develop a delayed sleep phase (DSP), others will fulfill the criteria for the diagnosis of delayed sleep phase disorder (DSPD). All previous studies have however not separated DSP from DSPD, and, as a result, the prevalence and associated factors are largely unknown for the two conditions individually. We estimated the prevalence of DSP and DSPD in a Swedish cohort of adolescents and young adults. We also investigated associated factors in the two conditions relative to each other and individuals with no delayed sleep phase. A questionnaire regarding sleep patterns, demographics, substance use/abuse, and symptoms of depression, anxiety, worry, and rumination was sent to 1000 randomly selected participants (16–26 years of age) in Uppsala, Sweden (response rate = 68%). DSP was defined as a late sleep onset and a preferred late wake up time. The DSPD diagnosis was further operationalized according to the Diagnostic and Statistical Manual of Mental Disorders, Edition 5 (DSM-5) criteria including insomnia or excessive sleepiness, distress or dysfunction caused by the delayed sleep phase and that the sleep problem had been evident for 3 months. DSP occurred at a frequency of 4.6% and DSPD at a frequency of 4% in the investigated cohort. DSP was more common in males and was associated with not attending educational activity or work, having shift work, nicotine and alcohol use and less rumination. DSPD was equally common in males and females and was associated with not attending educational activity or work and with elevated levels of anxiety. Both DSP and DSPD appear to be common in adolescents and young adults in this Swedish cohort. No educational activity or work was associated with both DSP and DSPD. However, there were also apparent differences between the two groups in shift work, substance use and mental health, relative to persons with no delayed sleep phase. Thus, it seems reasonable to assess DSP and DSPD as distinct entities in future studies.

Dim light melatonin onset (DLMO) is defined as the start of the melatonin production in the evening during dim light conditions and has become a reliable phase marker of the circadian clock. The aim of the study was to investigate DLMO and its association with sleep timing and diurnal preferences in healthy working adults during real-life conditions. Fourteen adults were investigated. A sleep diary was kept during the preceding week, but no fixed sleep–wake schedule was implemented. Diurnal preferences were measured with the Horne–O¨ stberg Morningness–Eveningness Questionnaire. DLMO was defined as the time point when melatonin in saliva exceeded a threshold of 3 ng/L. Results showed that DLMO appeared in the expected time interval but was not significantly associated with sleep timing or diurnal preference. The results illustrate the complexity of monitoring sleep patterns in real-life settings.

This article reports the development of a treatment protocol, based on cognitive behavioral therapy (CBT) principles, for delayed sleep–wake phase disorder (DSWPD). The protocol consists of psycho-education, presenting a CBT model for DSWPD, case formulation, motivational interviewing, registering sleep in a diary, strategies to improve the rhythm of sleep and wakefulness, relaxation training, cognitive restructuring, strategies to cope with daytime symptoms, constructing an individualized CBT program, and learning how to deal with relapses. Qualitative data, focusing on how the patients perceived the protocol, were collected within the realm of a trial exploring the efficacy of the protocol. These findings highlighted several advantages but also disadvantages of the therapy. It is our hope that this paper might act as a platform for further clinical work and future research efforts in patients with DSWPD.

Purpose: The aim of the study was to explore the communication experiences of key communications partners (CPs) of individuals receiving home mechanical ventilation (HMV), with particular emphasis on the possibilities, difficulties and limitations CPs experienced in communication, possible support given to facilitate communication and exploring what made a skilled communicator. Method: A qualitative research design using interviews was used. The participants included 19 key CPs of individuals receiving HMV. Results: The analysis resulted in five themes: Encountering communication limitations, Functional communication strategies, Being a communication facilitator, Role insecurity and Emotional reactions and coping. The findings revealed that CPs needed to develop partly new reference frames for communication. In particular, participants emphasised the need to understand and interpret subtle details in the communicative interaction. Conclusions: The findings are discussed in the light of previous research, in particular an earlier study exploring another perspective; the ventilator-supported individuals' experiences of communication. Issues relating to the educational needs of CPs of individuals receiving HMV are discussed. The results are intended to enhance understanding of the challenges that individuals receiving HMV and their CPs face with communication, which should be of relevance not only to speech therapists, but for all healthcare practitioners in the field of HMV.

BACKGROUND:

Short periods of sustained increase in airway pressures (Press(up)) are believed to re-open lung areas that collapsed upon induction of anaesthesia. Recruitment of alveolar surface is usually assessed in terms of changes in the pressure-volume (PV) curve. The purpose of this study was to analyse PV-curves before and after a Press(up) and to ascertain whether such changes are compatible with the concept of recruitment of lung volume.

METHODS:

During ketamine anaesthesia, 12 healthy piglets were subjected to a Press(up) with end-expiratory pressure (PEEP) of 12 cmH2O and end-inspiratory pressure of 40 cmH2O. Before and after Press(up), PV-curves were obtained from a slow insufflation of 630 ml at zero PEEP (ZEEP).

RESULTS:

Compliance was non-linear both before and after Press(up) increasing up to 300 ml and sharply decreasing thereafter. After Press(up), the entire compliance curve was shifted to a higher absolute level. Up to 100 ml and a pressure level corresponding to the lower inflection point on the PV-curve (LIP), compliance was higher before Press(up). No effects on blood gases could be observed.

CONCLUSION:

If the similar shape of the compliance curve corresponds to a similar chain of re-opening and overdistension events, this would imply that all volume gained by Press(up) is lost within 10 min, without explaining the higher absolute compliance following Press(up). We speculate that a) re-opening of rapidly collapsing small airways determines the initial compliance increase; b) the lower compliance after Press(up) until LIP indicates reduced intratidal re-opening of lung regions; and c) changes in bronchomotor tone induced by Press(up) raise the absolute compliance, with a similar scenario of alveolar and small airway recruitment now taking place but at different degrees of airway stiffness.

Ventilation with decelerating inspiratory flow is known to reduce the dead space fraction and to decrease PaCO2. Constant inspiratory flow with an end-inspiratory pause (EIP) is also known to increase the removal of CO2. The aim of the study was to elucidate the effect of the pause/no-flow period while both the pattern and rate of inspiratory flow was unchanged, and when the lung was ventilated with sufficient PEEP to prevent end-expiratory collapse. Surfactant depleted piglets were assigned to decelerating or constant inspiratory flow with 24 breaths per minute (bpm) or 12 bpm, or to constant flow, without and with an end-inspiratory pause of 25%. By adding an EIP the total time without active inspiratory flow of the respiratory cycle was kept unchanged. Gas exchange, airway pressures, functional residual capacity (using sulfurhexafluoride) and haemodynamics (thermo-dye indicator dilution technique) were measured. Irrespective of ventilatory frequency, PaCO2 was lower and serial dead space reduced with decelerating flow, compared with constant inspiratory flow. With an end-inspiratory pause added to constant inspiratory flow, serial dead space was reduced but did not decrease PaCO2. The results of this study corroborate the assumption that total time without active inspiratory flow is important for arterial CO2-tension.

Introduction: Nocturnal enuresis and sleep disordered breathing are common childhood problems that are reported to be associated with each other. Sleep disordered breathing is often found in children with upper airway obstruction and, according to some studies, its presence is associated with an increased risk of nocturnal enuresis. Respiration during sleep in children with therapy-resistant enuresis, but no history of snoring or sleep apneas, has previously been investigated, and subclinical signs of disordered respiration were found in this group. However, sleep disordered breathing in enuretic children without a history of snoring or sleep apneas has not been thoroughly studied before.

Aim: To evaluate sleep disordered breathing in enuretic children and compare them with healthy control children.

Subjects and methods: Children aged 8-13 years with nocturnal enuresis were included. Exclusion criteria were: daytime incontinence, on-going anti-enuretic treatment, and concomitant urological, endocrinological, nephrological or psychiatric disorders. Twenty children (19 boys and 1 girl) suffering from therapy-resistant nocturnal enuresis, and 21 healthy controls (18 boys and 3 girls) underwent one night of polygraphic sleep registration focused on respiratory variables. The registration included electroencephalography as well as assessment of respiratory movements, nasal airflow and oxygen saturation; it was performed with a portable sleep device at the subjects' homes. In addition to this, OSA 18, a health-related quality of life instrument, was used to evaluate subjective issues related to sleep and breathing.

Results: The mean apnea hypopnea index values were 0.96 +/- 0.8 for the patient group and 0.46 +/- 0.4 for the control group. The oxygen desaturation index was slightly higher for the children with nocturnal enuresis compared with the healthy controls (P = 0.05). No other differences were found in the respiratory variables. Both groups of children showed low levels of arousals (Summary Table). The enuretic children reported significantly more subjective sleep disturbances and a lower quality of life than their healthy peers.

Discussion: This was the first controlled study of sleep disordered breathing in children with nocturnal enuresis. One limitation of the study was that some variables were known to be underestimated when scoring polygraphic data. The apnea hypopnea index was such a variable and was indeed lower than in a previous study.

Conclusion: No major differences in respiration during sleep were found between enuretic children and controls.

AimThere have not been any continence-specific measurement tools in Swedish that have allowed clinicians to investigate the quality of life (QoL) in children with bladder dysfunction. This study evaluated the QoL in Swedish children with nocturnal enuresis and tested the reliability of a Swedish translation of the Paediatric Incontinence Questionnaire (PinQ). MethodsThis prospective study comprised 46 children aged six to 18 years with nocturnal enuresis, who completed the PinQ after it was translated into Swedish. It was completed twice by 33 patients, and these responses were included in the test-retest evaluation. ResultsThe self-reported mean sum score for the whole group was 26.3 13.37 (range: 5-58), and the most affected domains were social relations with peers and self-esteem. The highest individual scores were four, three or two for 71.7%, 17.4% and 10.9% of the study population, respectively. Cronbach's alpha was 0.87 for the whole questionnaire, indicating good internal consistency. The test-retest stability was excellent, with an intra-class correlation coefficient of 0.76. ConclusionChildren with nocturnal enuresis had impaired self-esteem, and their impaired QoL affected their relationships with friends. The Swedish version of the PinQ proved to be a reliable tool that will be used in further studies.