Other causes which have not yet been identified are likely as well. Different systems for classifying lissencephaly exist. One major distinction is "classic" (type I) vs. "cobblestone" (type II), but some systems add additional forms that fit into neither of these categories. Some types of lissencephaly are described below (OMIM numbers are included where available):

Treatment
Treatment for those with lissencephaly is symptomatic and depends on the severity and locations of the brain malformations. Treatment is tailored towards the symptoms of the individual. Therapies for lissencephaly are to deal with the symptoms as the syndrome is congenital. Supportive care may be needed to help with comfort and nursing needs. Seizures may be controlled with medication and hydrocephalus may require shunting. If feeding becomes difficult, a gastrostomy tube may be considered. There are a number of organisations that raise awareness and funding for rare disabilities such as lissencephaly. They also seek to increase the quality of life for individuals living with related disabilities. In the United States, these organizations include Arc of the United States, National Organization for Rare Disorders, and March of Dimes. Prognosis
The prognosis for children with lissencephaly varies depending on the malformation and severity of the syndrome. Many individuals remain at a 3–5 month developmental level. Life expectancy is short and many children with lissencephaly will die before the age of 10. Some children with lissencephaly will be able to roll over, sit, reach for objects, and smile socially. Aspiration and respiratory disease are the most common causes of illness or death.
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.