Study design, materials and methods
A survey of 186 patients with OAB syndrome was conducted to determine the presence of nocturnal enuresis in childhood and age at which bladder control was obtained. There were 168 women and 18 men among the surveyed patients. OAB syndrome with presence and absence of urgency incontinence was determined in 114 and 72 patients respectively.
Only 39 (21%) out of 186 patients reported about the presence of nocturnal enuresis in childhood. There were 30 women and 9 men among them that amounted to 17.9% and 50% of all respondents respectively. Therefore the frequency of nocturnal enuresis in childhood in men with OAB syndrome was significantly higher than in women (p = 0.004). When analyzing the frequency of nocturnal enuresis, no dependence on the symptoms of the OAB syndrome was detected. The incidence of nocturnal enuresis among patients with and without urgency incontinence was 19.4% and 21.9% respectively (p>0.1).
Only 3 (7.7%) out of 39 patients who had nocturnal enuresis in childhood indicated that it is still present. In the remaining 36 patients, nocturnal enuresis stopped at the age of 5 to 16 years, and in most of the patients (66.7%) this occurred no later than at the age of 10 years. There were no differences between the age of termination of nocturnal enuresis in women and men (9.29 ± 0.57 and 9.50 ± 1.31 years respectively, p> 0.1). At the same time, differences in the age of termination of nocturnal enuresis in patients depending on the symptoms of the OAB syndrome were noted. It turned out that only 12 (52.1%) out of 23 patients with urgency incontinence got rid of nocturnal enuresis before the age of 10, so did 12 (92.3%) out of 13 patients with “dry” OAB syndrome (p = 0.037).
Interpretation of results
Thus, the age of termination of nocturnal enuresis does not depend on the sex of the patient, but is associated with the symptoms of the OAB syndrome instead. Therefore, the later the nocturnal enuresis stopped, the higher was the probability of developing urgency incontinence in the adulthood. This can be explained by the fact that the mechanisms of the pathogenesis of nocturnal enuresis and OAB syndrome are essentially the same, namely, impairment of the nervous regulation of sensitivity and contractile activity of the bladder during the filling phase. The very fact of the presence of nocturnal enuresis in childhood suggests that the patient has an inborn "abnormality" of urinary reflex. Recently appeared data indicate that these disorders can be not only functional, but also might be associated with genetically determined morphological defects, in particular, changes in the density of receptors in the bladder and spinal cord. That is why such children might be predisposed in adulthood to the development of the OAB syndrome. The more pronounced these disorders are in a child with nocturnal enuresis, the later urinary reflex will be normalized and the bladder control will be restored. However, with the development of the OAB syndrome in adulthood, the disease occurs in such a patient in a more severe form, that is, accompanied by urgent urinary incontinence. However, if OAB syndrome occurs in such patients in adulthood, then it is much more often accompanied by urgency urinary incontinence.