MLIS2
Microlissencephaly Type B or Barth microlissencephaly syndrome: is a microlissencephaly with thick cortex, severe cerebellar and brainstem hypoplasia. The Barth-type of MLIS is the most severe of all the known lissencephaly syndromes.This phenotype consists of polyhydramnios (probably due to poor fetal swallowing), severe congenital microcephaly, weak respiratory effort, and survival for only a few hours or days. Barth described two siblings with this type as having a very low brainweight, wide ventricles, a very thin neopallium, absent corpus callosum and absent olfactory nerve. MLIS3
Microlissencephaly with intermediate cortex and abrupt anteroposterior gradient

MLIS4
Microlissencephaly with mildly to moderately thick (6–8 mm) cortex, callosal agenesis

Presentation
Microlissencephalic patients suffer from spasticity, seizures, severe developmental delay and intellectual disabilities with survival varying from days to years. Patients may also have dysmorphic craniofacial features, abnormal genitalia, and arthrogryposis.Microlissencephaly may arise as a part of Baraitser-Winter syndrome which comprises also ptosis, coloboma, hearing loss and learning disability. Moreover, it is the distinct developmental brain abnormality in "microcephalic osteodysplastic primordial dwarfism" (MOPD1). Microlissencephaly may be accompanied by micromelia as in Basel-Vanagaite-Sirota syndrome (a.k.a. Microlissencephaly-Micromelia syndrome). Pathophysiology
The genetic basis and pathophysiology of microlissencephaly are still not completely understood. Most cases of microlissencephaly are described in consanguineous families suggesting an autosomal recessive inheritance. Mutation of RELN gene or CIT could cause MLIS. Human NDE1 mutations and mouse Nde1 loss lead to cortical lamination deficits, which, together with reduced neuronal production cause microlissencephaly. Homozygous frameshift mutations in NDE1 gene was found to cause microlissencephaly with up to 90% reduction in brain mass and seizures starting early in life.
Some other disease-causing genes include: KATNB1 and WDR62. It is hypothesized that the KATNB1-associated microlissencephaly is the result of a combined effect of reduced neural progenitor populations and impaired interaction between the Katanin P80 subunit (encoded by KATNB1) and LIS1 (a.k.a. PAFAH1B1), a protein mutated in type 1 lissencephaly. Missense mutation in ACTG1 gene was identified in three cases of microlissencephaly. ACTG1 is the same gene that, when mutated, causes Baraitser-Winter syndrome. A loss-of-function mutation in the Doublesex- and Mab-3–Related Transcription factor A2 (DMRTA2, also known as DMRT5) gene has been reported in a case of microlissencephaly, implicating DMRTA2 as a critical regulator of cortical neural progenitor cell dynamics.Microlissencepahly is considered a tubulinopathy (tubulin gene defect) i.e. is caused by mutation in tubulin genes, mainly TUBA1A and less commonly TUBB2B, TUBB3, TUBA3E and TUBG1. Central pachygyria, polymicrogyria are more commonly seen in patients with defects in TUBB2B, TUBB3, and TUBB5. This implys the critical role of microtubule cytoskeleton in the pathophysiology of microlissencephaly as well as other neuronal migration disorders.Congenital infections like cytomegalovirus are also known to cause microlissencephaly.Both microlissencephaly and microcephaly with simplified gyral pattern result from either decreased stem cell proliferation or increased apoptosis in the germinal zone of the cerebral cortex. Diagnosis
Microlissencephaly can be diagnosed by prenatal MRI. MRI is better than ultrasound when it comes to detecting microlissencephaly or MSGP prenatally. The ideal time for proper prenatal diagnosis is between the 34th and 35th gestational week which is the time when the secondary gyration normally terminates.