Prospective controlled studies on the treatment of enuresis with desmopressin (DDAVP) indicate that cure rates (complete dryness) while on therapy are markedly lower than are response rates (decrease in wet nights). In an attempt to explain this discrepancy, we analyzed the etiological mechanisms for enuresis and found evidence that most children are not cured by DDAVP because their nocturnal wetting is not actually caused by the defect which DDAVP therapy aims to cure: low nocturnal vasopressin secretion with high nocturnal urinary output. Our study suggested that an arrest in the normal development of two separate areas of the central nervous system is necessary for enuresis to occur in many 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 observations about this condition and to explain why many patients react inconsistently to treatment aimed at a single etiology, yet eventually become dry.