Three main types of lissencephaly have been identified and although all types display the similar symptoms the pathogenesis of each type varies.The genes associated with lissencephaly are still being discovered; however, due to advances in genetics individual genes are being identified as the cause of lissencephaly. Mutations in LIS1, DCX (doublecortin), ARX(aristaless related homeobox), RELN have all been identified to cause lissencephaly. Viral infections can also cause lissencephaly.The known genetic and viral causes are listed below:

LIS1
LIS1 (also known as PAFAH1B1) is the most widely studied. LIS1 is located on chromosome 17p13.3. LIS1 is integral in regulating the motor protein dynein which plays an important role in the movement of neuronal nuclei along microtubules. The mutation or deletion involving LIS1 is associated with both Isolated Lissencephaly Syndrome and Miller–Dieker syndrome. Miller-Dieker syndrome however, has additional deletions of adjacent genes on chromosome 17 causing facial and other congenital abnormalities and defects. This mutation full or deletion of chromosome 17p13.3 leads to inadequate neuronal migration due to LIS1 encoding for an enzyme that interacts with the microtubule protein dynein. LIS1 mutation or deletion is not inherited from a parent and thus recurrence is unlikely.A Chinese family with an autosomal dominant inheritance pattern and a mutation in this gene has been reported. DCX
DCX or doublecortin encodes for the doublecortin protein which is similar to LIS1 as it encodes a microtubule associated protein that is related to microtubule function and transport in developing neuronal processes.
However, with almost universal use of ultrasound in the developed world, many cases are now detected during pregnancy, giving the opportunity to deliver the baby before this catastrophic rupture of the membranes occurs. Vasa previa is diagnosed with ultrasound when echolucent linear or tubular structures are found overlying the cervix or in close proximity to it. Transvaginal ultrasound is the preferred modality. Color, power and pulsed wave Doppler should be used to confirm that the structures are fetal vessels. The vessels will demonstrate a fetal arterial or venous waveform. Alkali denaturation test detects the presence of fetal hemoglobin in vaginal blood, as fetal hemoglobin is resistant to denaturation in presence of 1% NaOH. Tests such as the Ogita Test, Apt test or Londersloot test were previously used to attempt to detect fetal blood in the vaginal blood, to help make the diagnosis. These tests are no longer widely used in the US, but are sometimes used in other parts of the world. Also detection of fetal hemoglobin in vaginal bleeding is diagnostic. Treatment
It is recommended that women with vasa previa should deliver through elective cesarean prior to rupture of the membranes. Given the timing of membrane rupture is difficult to predict, elective cesarean delivery at 35–36 weeks is recommended. This gestational age gives a reasonable balance between the risk of death and that of prematurity. Several authorities have recommended hospital admission about 32 weeks. This is to give the patient proximity to the operating room for emergency delivery should the membranes rupture.