Abstract :
Neural tube defects (NTDs) constitute one of the most common malformations of human structure with a major public health burden (0.5-2/1000 pregnancies worldwide).1-3 They remain a preventable cause of still birth, neonatal and infant death, or significant lifelong handicaps. The underlying pathology is the consequence of a defect in the neurulation process very early in pregnancy, between 21 and 28 days after conception, leading to failure of the neural folds to fuse in the midline and form the neural tube.1 Secondary abnormal development of the mesoderm, responsible for forming the skeletal and muscular structures that cover the underlying neural structures, follows resulting in dysraphism, which indicates persistent continuity between the posterior neural ectoderm and cutaneous ectoderm. Based on embryological considerations and the presence or absence of exposed neural tissue, NTDs are classified as open or closed types. Cranial dysraphism (failure of cranial neural tube closure) includes anencephaly and encephaloceles, whereas spinal dysraphism (due to failure of caudal neuropore closure) is divided into open spinal dysraphisms (myelomeningocele, myelocele, hemimyelocele, and hemimyelomeningocele) and closed spinal dysraphisms. The latter can be associated with subcutaneous mass and includes lipomas with dural defect and meningocele.
