Pathophysiology of Enuresis
Enuresis’ pathophysiology is complex, consisting of the circadian rhythm (sleep & diuresis), the central nervous system (numerous receptors and neurotransmitters), plus bladder function imbalances. Urinary self-restraint or continence gets attained in three consecutive steps which are the bladder’s enlargement capacity, the sphincter muscles’ free or voluntary control as well as the micturition reflex’s voluntary control.
- The LC (locus coeruleus), which is a noradrenergic neuron group that’s in the upper pons tends to be vital for awakening or arousal from sleep where it overlaps both anatomically and functionally with the pontine micturition center, which tends to coordinate the micturition reflex.
- Also, the LC has axonal networks with hypothalamic cells which produce vasopressin. Thus, instabilities in this brainstem’s area may be the absent linkage to a merging pathogenic mechanism (Sinha, 2016).
Enuresis can as well result from:
a. Too much production of urine at night
- There is a lack or absence of nocturnal surge in plasma levels of the vasopressin or anti-diuretic hormone in enuretics as compared to the non-enuretic children, therefore, leading to relative nocturnal polyuria
b. Small bladder capacity
- Detrussor overactivity during sleep tends to have been observed in many enuretics resulting in a decrease or reduction in the bladder’s reservoir capacity
c. The child’s inability to wake up to a full bladder signals
- Enuretic children have a decreased arousal to a full bladder, i.e. before micturition occurs.
Sinha, R., & Raut, S. (2016). Management of nocturnal enuresis-myths and facts. World journal of nephrology, 5(4), 328.