Prospective controlled studies on the treatment of enuresis with desmo
pressin (DDAVP) indicate that cure rates (complete dryness) while on t
herapy are markedly lower than are response rates (decrease in wet nig
hts). In an attempt to explain this discrepancy, we analyzed the etiol
ogical mechanisms for enuresis and found evidence that most children a
re not cured by DDAVP because their nocturnal wetting is not actually
caused by the defect which DDAVP therapy aims to cure: low nocturnal v
asopressin secretion with high nocturnal urinary output. Our study sug
gested that an arrest in the normal development of two separate areas
of the central nervous system is necessary for enuresis to occur in ma
ny patients, yet cure of enuresis occurs if either developmental delay
is eliminated. This hypothesis of a dual developmental delay helps to
unify many diverse and often seemingly contradictory scientific obser
vations about this condition and to explain why many patients react in
consistently to treatment aimed at a single etiology, yet eventually b
ecome dry.