Spina Bifida in Infants

spina bifida During the course of any pregnancy, both mother and child are subjected to significant risks in the form of pregnancy complications. However, one pregnancy complication that many parents fail to consider sufficiently soon enough at the outset of a pregnancy is the possibility of the birth defect spina bifida. Spina bifida, which is a congenital malformation in the embryo’s nascent attempt to develop a cerebral-spinal system, leaves infants with varying degrees of spinal and nerve damage as these fetal developments grow into the pre-existing spinal opening caused by spina bifida in the first weeks of pregnancy, which fails to fully close the neural tube of the embryo that later forms the infant’s lumbar region.

Reducing Fetal Risks of Spina Bifida

Specifically, reliable risk mitigation of the childbirth defect spina bifida via maternal consumption of folic acid daily at a dose of 0.4 grams should commence twelve weeks prior to desired date of conception, per the recommendation of the FDA. This spina bifida risk reduction regimen is also augmented by the additional screening recommendation, and occasional law depending on state-jurisdiction, requiring expectant mothers to undergo alpha-fetoprotein serum testing early in their pregnancies to determine whether or not spina bifida is suspected in a given pregnancy. In addition to a maternal serum test, fetal ultrasounds are deployed by obstetricians to visually inspect for visible abnormalities in the spinal growth of the fetus. In the uncommon event that spina bifida is not diagnosed during pregnancy, the birth defect can also be confirmed upon visual inspection of the newborn’s spinal column, as well as via x-rays or other full body scans (MRIs or CT scans).

The Suspected Causes of Spina Bifida

Spina bifida is generally thought to be caused by genetics in combination with a variety of environmental factors. Environmental factors such as diabetes, being overweight, having a folic acid deficiency, and using prescription medicines that can cause birth defects during pregnancy, such as prescriptions used in the treatment of epilepsy, depression, and certain acne medications, have all been found to contribute to increased risks of a fetus developing spina bifida. While its genetic origins are still unknown, spina bifida’s progression as a condition occurs when the neural tube of the embryotic fetus fails to fully close upon itself in the first four weeks of gestation. In short, spina bifida developments nearly within the first month of pregnancy in a limited number of pregnancies. Per the CDC, the risk factors associated with increased likelihood of an embryo developing spina bifida include:
  • Folate deficiencies in pregnant or soon to be pregnant women, or the inability to take 400mcg of vitamin B-9 both twelve weeks prior and twelve weeks after conception
  • Maternal health problems, including obesity and diabetes
  • Paternal and maternal history of pregnancy resulting in neural tube deformations
  • Overexposure or exposure to high body temperatures by a pregnant mother in the first trimester of a pregnancy
  • Certain prescription drugs, if taken immediately prior to, during, or following conception into the first trimester of a pregnancy, pose increased risks for the possibility of infant spina bifida. Specifically, the CDC and others have counter-indicated certain anti-epileptic medications for women who may become or expect to become pregnant, as these and other prescription medications stymie the body’s metabolism of folic acid and folate.
  • Specifically, carbamazepine (brand names including Tegretol, Carbatrol, Epitol, and Equetrol) and valporic acid (brand names including Stavzor, Depacon, Depakene, or Depakote) are both anti-epilepsy medications noted by the CDC as increasing infant spina bifida rates as high as seven and double the rest of the population
  Resources: http://www.mayoclinic.org/diseases-conditions/spina-bifida/basics/definition/con-20035356 http://www.cdc.gov/ncbddd/spinabifida/facts.html http://www.ncbi.nlm.nih.gov/pubmed/16249782
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