<unk>  occurs when local regions of the neural tube fail to fuse or there is failure in formation of the vertebral neural arches. Neural arch formation occurs in the first month of embryonic development (often before the mother knows she is pregnant). Some forms are known to occur with primary conditions that cause raised central nervous system pressure, raising the possibility of a dual pathogenesis. In normal circumstances, the closure of the neural tube occurs around the 23rd (rostral closure) and 27th (caudal closure) day after fertilization. However, if something interferes and the tube fails to close properly, a neural tube defect will occur. Medications such as some anticonvulsants, diabetes, obesity, and having a relative with<unk>  can all affect the probability of neural tube malformation. Extensive evidence from mouse strains with<unk>  indicates that there is sometimes a genetic basis for the condition. Human<unk> , like other human diseases, such as cancer, hypertension and atherosclerosis (coronary artery disease), likely results from the interaction of multiple genes and environmental factors. Research has shown the lack of folic acid (folate) is a contributing factor in the pathogenesis of neural tube defects, including<unk> . Supplementation of the mother's diet with folate can reduce the incidence of neural tube defects by about 70%, and can also decrease the severity of these defects when they occur. It is unknown how or why folic acid has this effect.<unk>  does not follow direct patterns of heredity as do muscular dystrophy or haemophilia. Studies show a woman having had one child with a neural tube defect such as<unk>  has about a 3% risk of having another affected child. This risk can be reduced with folic acid supplementation before pregnancy. For the general population, low-dose folic acid supplements are advised (0.4 mg/day).
Spina bifida
Teratoma
Hydranencephaly
Anencephaly
Lissencephaly
Exencephaly
Schizencephaly
Cranioschisis