Five statistically significant factors were uncovered as a PNE “syndrome”:
Bedwetting in deep sleep; 2. Changes in sleep architecture; 3. Alertness instability 4. Resistance to treatment; 5. Spontaneous self-cure or deterioration (appearance of other Parasomnias). The distribution of sleep stages in PNE were different from the control: Type 1: The first cycle was longer with a predominance of stage 4. Type 2: Predominance of stage 2 with frequent awakenings, and Type 3: Disorganized sleep structure. Probabilities of bedwetting (B.) were dependent on the length of each stage: stage 2 – 26.7%, stage 3 – 31.2%, stage 4 – 35.7%, REM – 6.4%.
After an enuretic (E) event sleep stages switched to another stage in 64.7% of the cases (mostly to REM or awake) within a few minutes, thus, bedwetting occurred predominantly between stages. Enuretic event had several “forerunning” characteristics and was therefore predictable: delta wave outbursts in brain activity on EEG, high spontaneous SGR( skin reaction), changes in heart rate variability, and changes in the body movements.
What was amazing that after the act of enuresis (bedwetting), the sleep structure and EEG “normalized”.
Repeated sleep studies after 6 months of dry period due to “self-cure” or treatment were found to be identical to the control.
Conclusion: The nature of Primary Enuretic Syndrome reflects involvement of the sleep-wake mechanisms in its genesis. “Normalization” of sleep structure after an enuretic episode and resistance to suppression, and “self-cure” suggest that bedwetting could have an initially protective (compensatory or adaptive) function as a physiological sleep “switch” or “stabilizer” to “offset” immature sleep mechanisms.
The Offset hypothesis of Enuresis (bedwetting) underlies initially adaptive function of bedwetting. Treatment of bedwetting should be focused on the correction of underlying sleep problems. Further research is needed to evaluate whether other Parasomnias might also have adaptive functions.