Children under substantial stress, particularly in their home environment, frequently engage in bedwetting, in order to alleviate the stress produced by their surroundings. Trauma can also trigger a return to bedwetting (secondary enuresis) in both children and adults. It is not bedwetting that increases the chance of criminal behavior, but the associated trauma. For example, parental cruelty can result in "homicidal proneness". Causes
The aetiology of NE is not fully understood, although there are three common causes: excessive urine volume, poor sleep arousal, and bladder contractions. Differentiation of cause is mainly based on patient history and fluid charts completed by the parent or carer to inform management options.Bedwetting has a strong genetic component. Children whose parents were not enuretic have only a 15% incidence of bedwetting. When one or both parents were bedwetters, the rates jump to 44% and 77% respectively.These first two factors (aetiology and genetic component) are the most common in bedwetting, but current medical technology offers no easy testing for either cause. There is no test to prove that bedwetting is only a developmental delay, and genetic testing offers little or no benefit. As a result, other conditions should be ruled out. The following causes are less common, but are easier to prove and more clearly treated:In some bed-wetting children there is no increase in ADH (antidiuretic hormone) production, while other children may produce an increased amount of ADH but their response is insufficient. Individuals with reported bedwetting issues are 2.7 times more likely to be diagnosed with Attention deficit hyperactivity disorder.
Acropectoral syndrome is an autosomal dominant skeletal dysplasia syndrome affecting the hands, feet, sternum, and lumbosacral spine. A recently proposed candidate gene for preaxial polydactyly is LMBR1, encoding a novel transmembrane receptor, which may be an upstream regulator of SHH. The LMBR1 gene is on human chromosome 7q36. Presentation
Some individuals have preaxial polydactyly in the feet (unilateral in one, bilateral in 13), consisting of a small extra biphalangeal toe, in most cases with an associated rudimentary extra metatarsal, lying in a soft tissue web between the hallux and second toe. In some cases, this was accompanied by hypoplasia of the head of the first metatarsal and absence of both phalanges of the hallux. Genetics
The cytogenetic location is 7q36 and genomic coordinates are GRCh37:147,900,000 - 159,138,663 (NCBI). Mapping of this syndrome was done by Dundar and coworkers in 2001. They showed that this phenotype was linked to a 6.4-cM region of 7q36 flanked by the EN2 gene and the marker D7S2423. Dundar and coworkers characterized and mapped acropectoral syndrome and also showed it was unrelated to acropectorovertebral syndrome. The mapping showed that the acropectoral locus was in a region where preaxial polydactyly and triphalangeal thumb-polysyndactyly had previously been mapped. This study was important because it expanded the range of phenotypes that are connected to this locus. Previously, preaxial polydactyly and sternal defects have been linked to ectopic expression of the gene Sonic hedgehog Shh in limbbud and lateral plate mesoderm during development in mice.